AIM:To investigate whether melatonin can ameliorate acute myocardial infarction(AMI)by in⁃hibiting ferroptosis.METHODS:H9C2 cells were cultured in AnaeroPack system with low sugar and serum-free medium for 10 h to con...AIM:To investigate whether melatonin can ameliorate acute myocardial infarction(AMI)by in⁃hibiting ferroptosis.METHODS:H9C2 cells were cultured in AnaeroPack system with low sugar and serum-free medium for 10 h to construct a cell model of AMI.Then cells were treated with melatonin and ferroptosis inducer erastin.The cell activity,reactive oxygen species(ROS),lipid peroxidation,mitochondrial membrane potential(MMP),and ferroptosis related protein expression were detected.A rat model of AMI induced by isoprenaline(ISO)injection was established to evaluate the effects of melatonin,in which the myocardial infarction size,cardiac injury,pathological changes,oxidative stress,iron ion and ferroptosis related protein expression were examined.RESULTS:Melatonin decreased the oxidative stress,lipid peroxidation and expression of ferroptosis protein in cardiomyocytes induced by hypoxia,but these effects could be impeded by the ferroptosis inducer erastin.Furthermore,in vivo experiments,we also found that melatonin im⁃proved the myocardial infarction size,cardiac injury,pathological changes,oxidative stress,and alleviated iron ion accu⁃mulation and ferroptosis.CONCLUSION:The cardioprotective effects of melatonin in AMI are associated with the inhi⁃bition of ferroptosis.展开更多
OBJECTIVE To explore the mechanism of action of Qihuang Zhuyu formula(QHZYF)in improving depression after myocardial infarction(MI),with a focus on revealing its regulatory effect on the inflammatory response of the h...OBJECTIVE To explore the mechanism of action of Qihuang Zhuyu formula(QHZYF)in improving depression after myocardial infarction(MI),with a focus on revealing its regulatory effect on the inflammatory response of the heart and brain.METHODS The active ingredients of QHZYF and the action targets for intervening in depression after MI were analyzed by using ultra-performance liquid chromatography-high-resolution mass spectrometry(UPLC-Q-TOF/MS)combined with network pharmacology and molecular docking.A rat model of depression after MI was established by ligation of the left anterior descending coronary artery combined with chronic restraint stress.Echocardiography was used to evaluate cardiac function,hematoxylin-eosin(HE)and Masson staining were used to evaluate myocardial injury,behavioral tests were used to detect melancholic behaviors,Nissl staining was used to evaluate hippocampal neuron injury.Western blot detection of tumor necrosis factor receptor 2(TNFR2),phosphatidylinositol-3-kinase(PI3K),phosphorylated seronine protein kinase(p-AKT),seronine protein kinase(AKT),tumor necrosis factor receptor 1(TNFR1),phosphorylated nuclear factorκB(p-NF-κB),and nuclear factorκB(NF-κB)in cardiac and hippocampal tissues was conducted.The levels of serum IL-6 and IL-10 were detected by enzyme-linked immunosorbent assay(ELISA),and the expression of TNFR1 and TNFR2 was detected by immunohistochemical technique(IHC).In vitro experiments,co-culture of rat cardiomyocyte line H9C2 cells and rat adrenal pheochromocytoma cell line with high differentiation PC12 cells was conducted,TNFR1 inhibitor(H398)and TNFR2 agonist(C-6His)were administered for intervention,and the expression of TNFR2,PI3K,p-AKT,AKT,TNFR1,NF-κB,p-NF-κB was detected by Western blot.Observe the apoptosis of cells by TUNEL staining,ELISA was used to detect the levels of IL-6 and IL-10 in the cell supernatant.RESULTS Network pharmacological analysis indicates that the TNF signaling pathway was a key target for the treatment of depression after MI with the QHZYF.In vivo experiments have confirmed that the intervention of QHZYF could significantly improve the cardiac function,myocardial tissue and hippocampal neuron structure damage of depressed rats after MI,and improve their depression-like behaviors.At the molecular level,the high-dose group of QHZYF significantly upregulated TNFR2,p-AKT/AKT,and IL-10 in cardiac and hippocampal tissues(P<0.01),and downregulated TNFR1,p-NF-κB/NF-κB and IL-6(P<0.01).In vitro experiments showed that the drug-containing serum of QHZYF significantly upregulated the expression of TNFR2,p-AKT/AKT and IL-10 in H9C2 and PC12 cells(P<0.01),downregulated the expression of TNFR1,p-NF-κB/NF-κB and IL-6(P<0.01),and significantly inhibited cell apoptosis(P<0.01).Furthermore,experiments on the combined application of H398 or C-6His further confirmed that its protective and anti-inflammatory effects were mediated by regulating the TNFR2/PI3K/AKT and TNFR1/NF-κB pathways.CONCLUSION QHZYF improves the homeostasis of heart and brain inflammation by regulating the TNF pathway,and ameliorates myocardial injury and depressive state in depressed rats after MI.展开更多
Objective To investigate the value of polar residual network(PResNet)model for assisting evaluation on rat myocardial infarction(MI)segment in myocardial contrast echocardiography(MCE).Methods Twenty-five male SD rats...Objective To investigate the value of polar residual network(PResNet)model for assisting evaluation on rat myocardial infarction(MI)segment in myocardial contrast echocardiography(MCE).Methods Twenty-five male SD rats were randomly divided into MI group(n=15)and sham operation group(n=10).MI models were established in MI group through ligation of the left anterior descending coronary artery using atraumatic suture,while no intervention was given to those in sham operation group after thoracotomy.MCE images of both basal and papillary muscle levels on the short axis section of left ventricles were acquired after 1 week,which were assessed independently by 2 junior and 2 senior ultrasound physicians.The evaluating efficacy of MI segment,the mean interpretation time and the consistency were compared whether under the assistance of PResNet model or not.Results No significant difference of efficacy of evaluation on MI segment was found for senior physicians with or without assistance of PResNet model(both P>0.05).Under the assistance of PResNet model,the efficacy of junior physicians for diagnosing MI segment was significantly improved compared with that without the assistance of PResNet model(both P<0.01),and was comparable to that of senior physicians.Under the assistance of PResNet model,the mean interpretation time of each physician was significantly shorter than that without assistance(all P<0.001),and the consistency between junior physicians and among junior and senior physicians were both moderate(Kappa=0.692,0.542),which became better under the assistance(Kappa=0.763,0.749).Conclusion PResNet could improve the efficacy of junior physicians for evaluation on rat MI segment in MCE images,shorten interpretation time with different aptitudes,also improve the consistency to some extent.展开更多
Background Increased levels of inflammatory markers have been documented in various settings of coronary artery disease. The vulnerability of coronary lesions in acute myocardial infarction(AMI) at the time of onset m...Background Increased levels of inflammatory markers have been documented in various settings of coronary artery disease. The vulnerability of coronary lesions in acute myocardial infarction(AMI) at the time of onset may be related to serum levels of C reactive protein(CRP) on admission, before CRP levels are affected by myocardial damage.Objective This study assessed the predictive value of CRP levels within six hours after the onset of acute anterior myocardial infarction with primary percutaneous coronary intervention(PCI).Methods The plasma CRP of 76 patients with first acute anterior myocardial infarction was measured within 6 hours after onset. They were divided into 2 groups: group 1( n =20) with elevated CRP( ≥0.3mg/dl ) on admission within 6 hours after onset and group 2( n =56) with normal CRP( <0.3mg/dl ) within 6 hours after onset. All patients were treated by primary PCI. The primary combined end points, including death due to cardiac causes, re MI related to the infarction artery(RIA) and repeat intervention of the RIA, and the restenosis rate were assessed in relation to CRP levels within 6 hours after onset. Left ventricular end diastolic volume index(EDVI),end systolic volume index(ESVI),and ejection fraction(EF) on admission and 6 month after the onset were assessed by left ventriculography. Changes in EDVI(ΔEDVI),ESVI(ΔESVI), and EF(ΔEF) were obtained by subtracting respective on admission values from corresponding 6 month follow up values. Results There were no significant differences in baseline characteristics between the two groups. The primary combined end points were significantly more frequent in group 1(20%) than those in group 2( 1.79% , P <0.01 ).In addition, restenosis rates were significantly higher in group 1 than in group 2(41.18% vs 16.07%, P<0.05). Group 1 showed greater increases in left ventricular volume and less improvement in EF compared with group 2(ΔEDVI 6.31 ±2.17 vs 3.29 ±9.46ml/m 2 , ΔESVI 5.92 ±2.31 vs 3.86 ±1.08ml/m 2 , ΔEF 1.92 ±0.47 vs 4.79 ±1.73% , P <0.05 , respectively).Conclusions CRP levels within 6 hours after the onset of AMI might predict adverse outcome after primary PCI and progressive ventricular remodeling within 6 month of AMI.展开更多
Objective To evaluate short time effects of primary percutaneous coronary intervention (pPCI) and rtPA thrombolysis+PCI (rtPA+PCI) on myocardial viability and ventricular systolic synchrony in AMI patients.Methods Eig...Objective To evaluate short time effects of primary percutaneous coronary intervention (pPCI) and rtPA thrombolysis+PCI (rtPA+PCI) on myocardial viability and ventricular systolic synchrony in AMI patients.Methods Eighty seven patients with first AMI were divided into two groups: group A ( n =42), pPCI group, the patients underwent PCI within 6h after onset of AMI; group B ( n =45), rtPA+PCI group, the patients underwent PCI after thrombolysis within 6h after onset of AMI; Myocardial viability was measured by 99m Tc MIBI SPECT. While, the parameters of cardiac function LVEF and ventricular systolic synchrony LVPS were measured by 99m Tc gated cardiac blood pool image on the first and the fourth weekend. Results (1) The peak CK MB was significantly lower in group A than that in group B( P <0.01 ). (2) Myocardial infarction area (MIA) was decreased and radioactivity counts in MIA was significantly increased in group A and B on the 4th weekend compared with that on the first weekend ( P <0.01 ), but there were no significant difference between group A and group B. (3) LVEF, LVPS were no significant difference between group A and group B.Conclusions (1)pPCI in acute myocardial infartion can limit infarct area, maintain ventricular systolic synchrony and improve ventricular function; (2) but, in those hospitals that there were no any condition for PCI, they should transfer the patients to central hospital for PCI after thrombolysis at the first time. It is beneficial to improve myocardial viability and ventricular systolic synchrony of AMI patients in short time.展开更多
Objective Comparative study on the feasibility,safety and outcome of transradial artery and transfemoral artery access for primary percutaneous coronary intervention (PCI) in patients with acute myocardial infarction(...Objective Comparative study on the feasibility,safety and outcome of transradial artery and transfemoral artery access for primary percutaneous coronary intervention (PCI) in patients with acute myocardial infarction(AMI).Methods Two hundred and eight patients with AMI episoded within 12 hours, male 159, female 49, age 58.9 ±11.9 (34～88)years, were randomly divided into transradial artery access for primary PCI (TRA pPCI) group of 106 cases and transfemoral artery access for PCI (TFA pPCI) group of 102 cases during Sept, 2000 to Aug, 2002. The protocols of the manipulation duration and the effect for TRA pPCI and TFA pPCI procedures were respectively compared, including the time of transradial artery puncture and the rate of puncture success at first time ; the time of guiding catheter engaging into target coronary ostium; the rate of patence in infarct related artery (IRA); total duration of manipulation and the successful rate.The incidence of complications such as bleeding, vessel injury,thrombi and embolism as well as the average stay of hospitalization between two groups was compared. The status and the incidance of vessel spasm were observed and the effect of medicine administration to prevent from and relieve the vascular spasm was evaluated. The time of Allen’s test before and after TRA pPCI , the inner diameter and the peak of blood velocity of the right and left radial artery were investigated with color Doppler vessel echography as well as the complications of radial artery were followed up 1 month after TRA pPCI procedure. Results Two cases in every TRA pPCI and TFA pPCI groups were crossed over each other because procedure of the transradial or transfemoral access was failure. One handred and six vessels (48 vessels in LAD,22 vessels in LCX and 36 vessels in RCA) associated with 28 vessels of total occlusion in TRA pPCI group and 102 vessels (51 vessels in LAD,18 veesles in LCX and 33 vessels in RCA) with 24 vessels in total occlusion in TFA pPCI group were angioplasticized . The successful rates of the first time puncture in access artery, the re patence IRA and pPCI were similar in TRA pPCI and TFA pPCI groups ( 93.4% vs 96.1% ;100% vs 100%; 96.2% vs 97.1% , P >0.05 ). There were no significant diffierence in the average time of puncture time of access artery ,engaging in target vessels of guiding catheters and the total procedure of PCI between the two groups ( 1.3 ±0.3s vs 1.2 ±0.3s ; 6.0 ±1.6min vs 5.8 ±0.9min ; 49.2 ±24.1min vs 46.5 ± 26.4min , P >0.05 ). The access artery complications such as bleeding ,hematoma and embolism as well the veneous thrombosis in TFA pPCI group were much more than those in TRA pPCI group(p< 0.01 ). Although slight artery spasm of 4.7% cases in TRA pPCI group was happened during the procedure of PCI , the procedure had being continued after administration of medicine to release the spasm. The time of Allen’s test ,diameter and the systolic velocity of blood in daul radial arteries were no significant change before and after pPCI.Conclusions The duration and effect by TRA pPCI for AMI with stable hemodynamics was similar to TFA pPCI. The complications such as of bleeding,vessel injury, thrombi and embolism by TRA pPCI were few, and it was unnecessary to discontinue the anticoagulation medicine. TRA pPCI might be selected as a access vessel for pPCI in AMI patients with stable hemodynamics.展开更多
Objective This study was to evaluate the efficacy and safety of a short acting reduced dose fibrinolytic regimen to promote early infarct related artery (IRA) patency for acyute myocardial infarction (AMI) patients re...Objective This study was to evaluate the efficacy and safety of a short acting reduced dose fibrinolytic regimen to promote early infarct related artery (IRA) patency for acyute myocardial infarction (AMI) patients referred for percutaneous coronary intervention (PCI).Methods Following aspirin and heparin, 166 patients were randomized to a 50 mg bolus of recombinant tissue type plasminogen activator(rt PA) or to a same volume sodium chloride injection followed by immediate primary PCI. The end points included patency rates on catheterization laboratory (cath lab) arrival, revascularization results when PCI was performed, complication rates, left ventricular function and restored patency rate following PCI. Results Patency on cath lab arrival was 64% with rt PA (34% TIMI 3,30% TIMI 2), while 31% of placebo (13% TIMI 3, 18% TIMI 2). There was no difference in the restored TIMI 3 rates of IRA between the two groups (85% vs 87%). No difference were observed in stroke or major bleeding. Left ventricular function was similar in both groups (52±9% vs 50±8%), but left ventricular ejection fraction fraction (LVEF) was higher with patent IRA (TIMI 3) on cath lab arrival than that of others (56±12% vs 48±10%).Conclusions Strategy thrombolytic regimens were compatible with subsequent PCI lead to more frequenc early recanalization (before cath lab arrival), which facilitates greater left ventricular function preservation with no augmentation of adverse events.展开更多
Aim Salvia miltiorrhiza Bunge （SM） and lignum dalbergiae odoriferae （DO） are both traditional Chi- nese medicine that have cardioprotective effects. Here, we further examined the combined effects of SM and DO on r...Aim Salvia miltiorrhiza Bunge （SM） and lignum dalbergiae odoriferae （DO） are both traditional Chi- nese medicine that have cardioprotective effects. Here, we further examined the combined effects of SM and DO on rat myocardial ischemia/reperfusion injury. The possible mechanism of SM and DO also were elucidated. Methods DO was divided into aqueous extract of lignum dalbergiae odoriferae （DOW） and lignum dalbergiae odoriferae oil （DOO）. Sprague-Dawley rats were randomized to seven groups： sham group, model group, treatment groups inclu- ding SM （10 g · kg^-1）, DOW （5 g · kg^-1）, DOO （0.5 ml · kg^-1）, SM ＋ DOW （10 g · kg^-1 ＋ 5 g · kg^-1）, SM ＋ DOO （ 10 g · kg^-1 ＋ 0. 5 ml · kg^-1）. Rats were pretreated with homologous drug for 7 days and then subjec- ted to 30 rain of ischemia followed by 180 rain of reperfusion. Electrocardiogram （ECG） and heart rate were moni- tored and recorded continuously. At the end of reperfusion, blood samples were collected to determine the serum levels of creatine kinase-MB （CK-MB） and lactate dehydrogenase （LDH）. Hearts were harvested to assess heart- body rate, infarct size and histopathological changes as well. Maximum and minimum effective points were deter- mined by measuring indicators associate with myocardial injury at different time-points of reperfusion （Smin, 15min, 30min, 45rain, 60min, 120min, 180min）. The potential therapeutic mechanism of SM and SM ＋ DOO were carried out by detecting superoxide dismutase （SOD）, malondialdehyde （MDA）, tumor necrosis factor-alpha （TNF-alpha） and interleukin 6 （IL-6）. Results The results showed SM and DO can ameliorate cardiac function respectively, and this cardioprotective effect was further strengthened by their combinations. Among all the combi- nations, SM ＋ DOO showed predominant potential to improve ECG and heart rate, reduce heart-body rate （28.5% ＋ 1.4% , P 〈 0.01 vs model） and myocardial infarct size （ 20.96% ＋ 1.61% , P 〈 0.01 vs model, P 〈 0.05 vs SM） , attenuate histopathological damage, decrease the levels of CK-MB and LDH （P 〈 0.01 vs model, P 〈 0.05 vs SM）. The maximum effective points of SM and SM ＋ DOO were 15min and 30rain respectively, and the minimum effective points of them were 180rain. In reducing serum level of MDA, TNF-alpha, IL-6 and increasing SOD activ- ity, SM ＋ DOO was similar to SM. Conclusion The results of this study indicated that SM ＋ DOO have combined effects that are highly effective than single pretreatment against myocardial ischemie reperfusion injury in rats. The possible mechanism of SM and DO were likely through its anti-oxidant and anti-inflammatory properties, and thus may be an effective and promising medicine for both prophylaxis and treatment of ischemic heart disease.展开更多
Erigeron multiradiatus(Lindl.)Benth.,has been used in Tibet folk medicine to treat various inflammatory diseases.The aim of this study was to investigate anti-myocardial ischemia and reperfusion(I/R)injury effect of c...Erigeron multiradiatus(Lindl.)Benth.,has been used in Tibet folk medicine to treat various inflammatory diseases.The aim of this study was to investigate anti-myocardial ischemia and reperfusion(I/R)injury effect of caffeoylquinic acids derivatives of E.multiradiatus(AE)in vivo and to explain underling mechanism.AE was prepared using the whole plant of E.multiradiatus and contents of 6 caffeoylquinic acid determined through HPLC analysis.Myocardial I/R were induced by left anterior descending coronary artery occlusion for 30 min followed by 24 h of reperfusion in rats.AE administration(10,20 and 40 mg·kg-1)inhibited I/R-induced injury as indicated by decreasing myocardial infarct size,reducing of CK and LDH activities and preventing ST-segment depression in dose-dependent manner.AE decreased cardiac tissue levels of pro-inflammatory factors TNF-αand IL-6 and attenuated leukocytes infiltration.AE was further demonstrated to significantly inhibit I-κB degradation,nuclear translocation of p-65 and phosphorylation of JNK.Our results suggested that cardioprotective effect of AE could be due to suppressing myocardial inflammatory response and blocking NF-κB and JNK activation pathway.Thus,caffeoylquinic acids might be the active compounds in E.multiradiatus on myocardial ischemia and be a potential natural drug for treating myocardial I/R injury.展开更多
OBJECTIVE To investigate the effects of astragaloside IV(which can be extracted from the traditional Chinese medicine Astragalus membranaceus)on lipid and glucose metabolism in acute myocardial infarction(AMI).METHODS...OBJECTIVE To investigate the effects of astragaloside IV(which can be extracted from the traditional Chinese medicine Astragalus membranaceus)on lipid and glucose metabolism in acute myocardial infarction(AMI).METHODS Model of heart failure(HF)after AMI was established with ligation of left anterior descending artery on Sprague-Dawley(SD)rats.The rats were divided into three groups:sham,model and astragaloside IV treatment group.Twenty-eight days after treatment(astragaloside IV,20 mg·kg-1 daily),hematoxylin-eosin(HE)staining was applied to visualize cardiomyocyte morphological changes.High performance liquid chromatography(HPLC)was performed to assess the contents of adenosine phosphates in heart.Positron emission tomography and computed tomography(PET-CT)was conducted to evaluate the cardiac glucose metabolism.Expressions of key molecules such as peroxisome proliferatoractivated receptor γ(PPARγ),sterol carrier protein 2(SCP2)and long chain acyl CoA dehydrogenase(ACADL)were measured by Western blotting and immunohistochemistry.Oxygen-glucose deprivation-reperfusion(OGD/R)-induced H9C2 injury cardiomyocyte model was adopted for potential mechanism research in vitro.RESULTS Treatment with astragaloside Ⅳ rescued hearts from structural and functional damages as well as inflammatory infiltration.Levels of adenosine triphosphate(ATP)and energy charge(EC)in astragaloside IV group were also up-regulated compared to model group.Further results demonstrated that critical enzymes both in lipid metabolism and glucose metabolism compro mised in model group compared to sham group.Intriguingly,astragalosideⅣcould up-regulate critical enzymes including ACADL and SCP2 in lipid metabolism accompanying with promoting effect on molecules in glycolysis simultaneously.Results on upstreaming signaling pathway demonstrated that astragaloside Ⅳ could dramatically increase the expres sions of PPARγ.In vitro study suggested the efficacy of astragalosideⅣcould be blocked by T0070907,a selective PPARγ inhibitor.CONCLUSION Astragaloside IV has cardioprotective effect in improving cardiac function and energy metabolism through regulating lipid and glucose metabolism.The effects may be mediated by PPARγ pathway.展开更多
In this work, we analyzed only the patients of the NSTEMI (non ST-segment elevation myocardial infarction) who arrived at the hospital within 12 h after symptoms started. Using NSTEMI follow-up data within, the charac...In this work, we analyzed only the patients of the NSTEMI (non ST-segment elevation myocardial infarction) who arrived at the hospital within 12 h after symptoms started. Using NSTEMI follow-up data within, the characteristics of the clinical data, the risk factor, and the blood tested in the hospital visit were analyzed for MACE (major adverse cardiac events) patients. MACE includes cardiac death, MI (myocardial infarction), Re-PCI, and CABG (coronary artery bypass graft). As a result, from the NSTEMI patients which can be followed up for over 12 m, NT-ProBNP (p=0.014) and age (p=0.045) are found to be the independent risk factors related to MACE. Accordingly, they can be useful for the diagnosis and prognosis for NSTEMI patients as a biomarker.展开更多
The YiQiFuMai powder injection （ YQFM）, a Traditional Chinese Medicine （TCM） prescription re-de- veloped based on the well-known TCM formula Sheng-maisan, showed a wide range of pharmacological activities in ca...The YiQiFuMai powder injection （ YQFM）, a Traditional Chinese Medicine （TCM） prescription re-de- veloped based on the well-known TCM formula Sheng-maisan, showed a wide range of pharmacological activities in cardiovascular diseases in clinic. However, its role in protection against myocardial ischemia/reperfusion （MI/R） injury has not been elucidated. The present study not only evaluated the eardioprotective effect of YQFM from MI/ R injury but also investigated the potential molecular mechanisms in vivo and in vitro. The mouse model of MI/R injury was induced by a transient vessel occlusion for 30 rain and reperfusion for 24 h. The myocardium infarct size, production of lactate dehydrogenase （LDH）, creatine kinase （CK）, TUNEL staining and easpase-3 activity were measured. AMPKeα and phospho-AMPKα was analyzed by Western blot. We further verified the protective effect and potential molecular mechanisms of YQFM in an in vitro model of simulated ischemia and reperfusion （ SI/ R） in H9c2 cardiomyocytes. Cell viability was determined, and cell apoptosis were measured by Hoechst 33342 staining and Flow cytometry. Mitochondrial membrane potential （△ψFm） was measured, and ATP content was quantified by biolumineseent assay. Expression of apoptosis-related proteins including Caspase-3, Bcl-2, Bax, AMPKα and phospho-AMPKα was analyzed by Western blot. AMPKoL siRNA transfection was also applied to the mechanism elucidation. YQFM significantly reduced myocardium infarct size and the production of LDH, CK in se- rum, and also produced a significant decrease of apoptotic index which was confirmed by TUNEL staining and the changes of caspase-3 activity. In addition, pretreatment with YQFM markedly improved cell viability and decreased LDH release. Moreover, YQFM inhibited H9c2 apoptosis, blocked the expression of easpase-3 and modulated Bcl- 2 and Bax proteins, leading to an increased mitochondrial membrane potential and cellular ATP content. Mechanis- tically, YQFM activated AMPK signaling pathways while pretreatment with AMPK inhibitor compound C and appli- cation of transfection with AMPKα siRNA attenuated the anti-apoptotie effect of YQFM. Our results indicated that YQFM could provide significant cardioproteetion against MI/R injury, and potential mechanisms might to suppres- sion of cardiomyocytes apoptosis at least in part through activating the AMPK signaling pathways.展开更多
OBJECTIVE To investigate the protective effect of salvianolic acid A(Sal A)on isoproterenol-induced myocardial infarction in mice and its possible mechanisms.METHODS The mice were subcutaneously injected with isopropr...OBJECTIVE To investigate the protective effect of salvianolic acid A(Sal A)on isoproterenol-induced myocardial infarction in mice and its possible mechanisms.METHODS The mice were subcutaneously injected with isopropranol(ISO 8mg·kg-1)to induce myocardial infarction and evaluated the myocardial protective effect of Sal A from mortality rate,electrocardiogram(ECG),heart function,myocardial infarction index,serum myocardial enzymes and explored its possible mechanisms from inflammatory,antioxidant and cells apoptosis.RESULTS Sal A can dose-dependently enhanced the heart function of myocardial infarction mice,reduced the heart index,inhibited the myocardial enzyme leakage,showed obvious myocardial protection effects.ELISA results showed that Sal A can reduce the expression of myocardial inflammatory cytokines such as IL-6,TNF-α.Western blotting confirmed that Sal A can increase the expression of anti-apoptotic proteins Bcl-2,reduce the expression of apoptosis protein Bax,and raise the phosphorylation level of PI3K and Akt.CONCLUSION Sal A have displayed significant protective effect against isoproterenol-induced myocardial infarction and its mechanism may be related to increasing of PI3K/Akt signal pathway and inhibition of cell apoptosis and inflammatory reaction.展开更多
Aim Baroreflex dysfunction is associated with a higher rate of sudden death after myocardial infarction （MI）. Ketanserin enhances baroreflex function in rats. The present work was designed to examine whether ketan- ...Aim Baroreflex dysfunction is associated with a higher rate of sudden death after myocardial infarction （MI）. Ketanserin enhances baroreflex function in rats. The present work was designed to examine whether ketan- serin improves the post-MI cardiac function and to explore the possible mechanism involved. Methods Spontane- ously hypertensive rats （SHR） were treated with ketanserin （0.3 mg · kg^-1 · d^-l）. Two weeks later, blood pres- sure and baroreflex function were measured, followed by a ligation of the left coronary artery. The expressions of ve- sicular acetylcholine transporter （VAChT） and α7 nicotinic acetylcholine receptor （α7-nAChR） in ischemic myo- cardium, angiogenesis, cardiac function, and left ventricular （LV） remodeling were evaluated subsequently. Re- sults Ketanserin significantly improved baroreflex sensitivity （0.62 ± 0. 21 vs. 0.34 ± 0. 12 ms/mmHg, P 〈 0.01 ） and vagal tonic activity （ heart rate changes in response to atropine, 54.8 ± 16.2 vs. 37.6 ± 13.4 b. p. m. , P 〈 0.01 ） without affecting the blood pressure or basic heart rate in SHR. Treatment of SHR with ketanserin promi- nently improved cardiac function and alleviated LV remodeling, as reflected by increases in the ejection fraction, fractional shortening, and LV systolic pressure as well as decreases in LV internal diameter and LV relative weight. The capillary density, vascular endothelial growth factor expression, and blood flow in the ischemic myocardium were significantly higher in the ketanserin-treated group. In addition, ketanserin markedly increased the expression of VAChT and α7-nAChR in ischemic myocardium. Conclusion Ketanserin improved post-MI cardiac function and angiogenesis in ischemic myocardium. The findings provide a mechanistic basis for restoring baroreflex function using ketanserin in the treatment of MI.展开更多
OBJECTIVE To investigate the protective effect of salvianolic acid A(Sal A)on isoproterenol-induced myocardial infarction in mice and its possible mechanisms.METHODS The mice were subcutaneously injected with isopropr...OBJECTIVE To investigate the protective effect of salvianolic acid A(Sal A)on isoproterenol-induced myocardial infarction in mice and its possible mechanisms.METHODS The mice were subcutaneously injected with isopropranol(ISO 8 mg·kg-1)to induce myocardial infarction and evaluated the myocardial protective effect of Sal A from mortality rate,electrocardiogram(ECG),heart function,myocardial infarction index,serum myocardial enzymes and explored its possible mechanisms from inflammatory,antioxidant and cells apoptosis.RESULTS Sal A can dose-dependently enhanced the heart function of myocardial infarction mice,reduced the heart index,inhibited the myocardial enzyme leakage,showed obvious myocardial protection effects.ELISA results showed that Sal A can reduce the expression of myocardial inflammatory cytokines such as IL-6,TNF-α.Western blotting confirmed that Sal A can increase the expression of anti-apoptotic proteins Bcl-2,reduce the expression of apoptosis protein Bax,and raise the phosphorylation level of PI3K and Akt.CONCLUSION Sal A have displayed significant protective effect against isoproterenol-induced myocardial infarction and its mechanism may be related to increasing of PI3K/Akt signal pathway and inhibition of cell apoptosis and inflammatory reaction.展开更多
Myocardial infarction(MI)is a disorder that lowers the lifespan and quality of life.Reperfusion treatment as early as possible is the most effective solution,with an increased focus on post-MI medication.In the recove...Myocardial infarction(MI)is a disorder that lowers the lifespan and quality of life.Reperfusion treatment as early as possible is the most effective solution,with an increased focus on post-MI medication.In the recovery process after MI,telocytes(TCs)appear to play an important role,which develops a large number of questions awaiting answers.Defining possible signaling mechanisms involved in recovery after MI may lead to identification the limits of current therapies,and development of new therapeutic solutions.Key words:telocytes;myocardial infarction;stem展开更多
Objective To explore the variation of treatment and outcomes for NSTEMI across different-level hospitals, which potentially influenced by unbalanced economy and disparate medical care.Methods The China AMI registry co...Objective To explore the variation of treatment and outcomes for NSTEMI across different-level hospitals, which potentially influenced by unbalanced economy and disparate medical care.Methods The China AMI registry consists of 108 hospitals across three levels (province, prefecture and county) throughout China.展开更多
Background and Objective Elevated serum levels of lipoprotein(Lp[a]) has recently been proposed as a marker of cardiovascular risk.We aimed to determine the role of Lp(a) on long-term clinical outcomes in patients wit...Background and Objective Elevated serum levels of lipoprotein(Lp[a]) has recently been proposed as a marker of cardiovascular risk.We aimed to determine the role of Lp(a) on long-term clinical outcomes in patients with ST elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI).展开更多
OBJECTIVE To explore the potential molecular mechanism of Shenlian(SL)on myocardial ischemia(MI)on the basis of network pharmacology.METHODS Firstly,the main active ingredients of SL were screened in the Traditional C...OBJECTIVE To explore the potential molecular mechanism of Shenlian(SL)on myocardial ischemia(MI)on the basis of network pharmacology.METHODS Firstly,the main active ingredients of SL were screened in the Traditional Chinese Medicine Integrated Database,and the MI-associated targets were collected from the DisGeNET database.Then,we used compound-target and target-pathway networks to uncover the therapeutic mechanisms of SL On the basis of network pharmacology analysis results,we assessed the effects of SL in MI rat model and oxygen glu⁃cose deprivation model of H9c2 cells and validated the possible molecular mechanisms of SL on myocardial injury in vivo and in vitro.RESULTS The network pharmacology results showed that 37 potential targets were recognized,including TNF-α,Bcl-2,STAT3,PI3K,and MMP2.The pathways revealed that the possible targets of SL were involved in the reg⁃ulation of inflammation and apoptosis signaling pathway.Then,in vivo experiments indicated that SL significantly reduced the myocardial infarction size of MI rats.Serum CK-MB,cTnT,CK,LDH,and AST levels were significantly decreased by SL(P<0.05 or P<0.01).In vitro,SL significantly increased H9c2 cell viability.The levels of inflammation factors including TNF-αand MMP2 were significantly decreased by SL(P<0.05 or P<0.01).TUNEL and Annexin V/propidium iodide assays indicated that SL could significantly decrease the cell apoptotic rate in vivo and in vitro(P<0.05 or P<0.01).The remarkable upregulation of anti-apoptotic Bcl-2 and downregulation of pro-apoptotic Bax protein level further confirmed this result.Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that the PI3K-Akt and JAK2-STAT3 pathways were significantly enriched in SL.Compared with the model group,SL treatment significantly activated the PI3K-Akt and JAK2-STAT3 pathways in vivo and in vitro according to Western blotting analyses.CONCLU⁃SION SL could protect the myocardium from MI injury.The underlying mechanism may be related to the reduction of inflammation and apoptosis by activating the PI3K/Akt and JAK2/STAT3 pathways.展开更多
Objective To assess the relationship of myocardial strain and torsion and quantitative heart function scores in patients with coronary heart disease after PTCA.Methods A total of 90 patients with coronary artery disea...Objective To assess the relationship of myocardial strain and torsion and quantitative heart function scores in patients with coronary heart disease after PTCA.Methods A total of 90 patients with coronary artery disease after PTCA were randomly divided into clinically normal heart function group(group A,n=43)and abnormal heart function group(group B,n=47),and 30 healthy people matched with age and gender as the control group(group C,n=30).展开更多
基金Supported by Guangdong Medical Research Foundation(No.A2024382)Guangdong Provincial Bureau of Traditional Chinese Medicine research project(No.20231321)Scientific Research Start Plan of Shunde Hospital,Southern Medical University(No.SRSP2022012,No.SRSP2022016)。
文摘AIM:To investigate whether melatonin can ameliorate acute myocardial infarction(AMI)by in⁃hibiting ferroptosis.METHODS:H9C2 cells were cultured in AnaeroPack system with low sugar and serum-free medium for 10 h to construct a cell model of AMI.Then cells were treated with melatonin and ferroptosis inducer erastin.The cell activity,reactive oxygen species(ROS),lipid peroxidation,mitochondrial membrane potential(MMP),and ferroptosis related protein expression were detected.A rat model of AMI induced by isoprenaline(ISO)injection was established to evaluate the effects of melatonin,in which the myocardial infarction size,cardiac injury,pathological changes,oxidative stress,iron ion and ferroptosis related protein expression were examined.RESULTS:Melatonin decreased the oxidative stress,lipid peroxidation and expression of ferroptosis protein in cardiomyocytes induced by hypoxia,but these effects could be impeded by the ferroptosis inducer erastin.Furthermore,in vivo experiments,we also found that melatonin im⁃proved the myocardial infarction size,cardiac injury,pathological changes,oxidative stress,and alleviated iron ion accu⁃mulation and ferroptosis.CONCLUSION:The cardioprotective effects of melatonin in AMI are associated with the inhi⁃bition of ferroptosis.
文摘OBJECTIVE To explore the mechanism of action of Qihuang Zhuyu formula(QHZYF)in improving depression after myocardial infarction(MI),with a focus on revealing its regulatory effect on the inflammatory response of the heart and brain.METHODS The active ingredients of QHZYF and the action targets for intervening in depression after MI were analyzed by using ultra-performance liquid chromatography-high-resolution mass spectrometry(UPLC-Q-TOF/MS)combined with network pharmacology and molecular docking.A rat model of depression after MI was established by ligation of the left anterior descending coronary artery combined with chronic restraint stress.Echocardiography was used to evaluate cardiac function,hematoxylin-eosin(HE)and Masson staining were used to evaluate myocardial injury,behavioral tests were used to detect melancholic behaviors,Nissl staining was used to evaluate hippocampal neuron injury.Western blot detection of tumor necrosis factor receptor 2(TNFR2),phosphatidylinositol-3-kinase(PI3K),phosphorylated seronine protein kinase(p-AKT),seronine protein kinase(AKT),tumor necrosis factor receptor 1(TNFR1),phosphorylated nuclear factorκB(p-NF-κB),and nuclear factorκB(NF-κB)in cardiac and hippocampal tissues was conducted.The levels of serum IL-6 and IL-10 were detected by enzyme-linked immunosorbent assay(ELISA),and the expression of TNFR1 and TNFR2 was detected by immunohistochemical technique(IHC).In vitro experiments,co-culture of rat cardiomyocyte line H9C2 cells and rat adrenal pheochromocytoma cell line with high differentiation PC12 cells was conducted,TNFR1 inhibitor(H398)and TNFR2 agonist(C-6His)were administered for intervention,and the expression of TNFR2,PI3K,p-AKT,AKT,TNFR1,NF-κB,p-NF-κB was detected by Western blot.Observe the apoptosis of cells by TUNEL staining,ELISA was used to detect the levels of IL-6 and IL-10 in the cell supernatant.RESULTS Network pharmacological analysis indicates that the TNF signaling pathway was a key target for the treatment of depression after MI with the QHZYF.In vivo experiments have confirmed that the intervention of QHZYF could significantly improve the cardiac function,myocardial tissue and hippocampal neuron structure damage of depressed rats after MI,and improve their depression-like behaviors.At the molecular level,the high-dose group of QHZYF significantly upregulated TNFR2,p-AKT/AKT,and IL-10 in cardiac and hippocampal tissues(P<0.01),and downregulated TNFR1,p-NF-κB/NF-κB and IL-6(P<0.01).In vitro experiments showed that the drug-containing serum of QHZYF significantly upregulated the expression of TNFR2,p-AKT/AKT and IL-10 in H9C2 and PC12 cells(P<0.01),downregulated the expression of TNFR1,p-NF-κB/NF-κB and IL-6(P<0.01),and significantly inhibited cell apoptosis(P<0.01).Furthermore,experiments on the combined application of H398 or C-6His further confirmed that its protective and anti-inflammatory effects were mediated by regulating the TNFR2/PI3K/AKT and TNFR1/NF-κB pathways.CONCLUSION QHZYF improves the homeostasis of heart and brain inflammation by regulating the TNF pathway,and ameliorates myocardial injury and depressive state in depressed rats after MI.
文摘Objective To investigate the value of polar residual network(PResNet)model for assisting evaluation on rat myocardial infarction(MI)segment in myocardial contrast echocardiography(MCE).Methods Twenty-five male SD rats were randomly divided into MI group(n=15)and sham operation group(n=10).MI models were established in MI group through ligation of the left anterior descending coronary artery using atraumatic suture,while no intervention was given to those in sham operation group after thoracotomy.MCE images of both basal and papillary muscle levels on the short axis section of left ventricles were acquired after 1 week,which were assessed independently by 2 junior and 2 senior ultrasound physicians.The evaluating efficacy of MI segment,the mean interpretation time and the consistency were compared whether under the assistance of PResNet model or not.Results No significant difference of efficacy of evaluation on MI segment was found for senior physicians with or without assistance of PResNet model(both P>0.05).Under the assistance of PResNet model,the efficacy of junior physicians for diagnosing MI segment was significantly improved compared with that without the assistance of PResNet model(both P<0.01),and was comparable to that of senior physicians.Under the assistance of PResNet model,the mean interpretation time of each physician was significantly shorter than that without assistance(all P<0.001),and the consistency between junior physicians and among junior and senior physicians were both moderate(Kappa=0.692,0.542),which became better under the assistance(Kappa=0.763,0.749).Conclusion PResNet could improve the efficacy of junior physicians for evaluation on rat MI segment in MCE images,shorten interpretation time with different aptitudes,also improve the consistency to some extent.
文摘Background Increased levels of inflammatory markers have been documented in various settings of coronary artery disease. The vulnerability of coronary lesions in acute myocardial infarction(AMI) at the time of onset may be related to serum levels of C reactive protein(CRP) on admission, before CRP levels are affected by myocardial damage.Objective This study assessed the predictive value of CRP levels within six hours after the onset of acute anterior myocardial infarction with primary percutaneous coronary intervention(PCI).Methods The plasma CRP of 76 patients with first acute anterior myocardial infarction was measured within 6 hours after onset. They were divided into 2 groups: group 1( n =20) with elevated CRP( ≥0.3mg/dl ) on admission within 6 hours after onset and group 2( n =56) with normal CRP( <0.3mg/dl ) within 6 hours after onset. All patients were treated by primary PCI. The primary combined end points, including death due to cardiac causes, re MI related to the infarction artery(RIA) and repeat intervention of the RIA, and the restenosis rate were assessed in relation to CRP levels within 6 hours after onset. Left ventricular end diastolic volume index(EDVI),end systolic volume index(ESVI),and ejection fraction(EF) on admission and 6 month after the onset were assessed by left ventriculography. Changes in EDVI(ΔEDVI),ESVI(ΔESVI), and EF(ΔEF) were obtained by subtracting respective on admission values from corresponding 6 month follow up values. Results There were no significant differences in baseline characteristics between the two groups. The primary combined end points were significantly more frequent in group 1(20%) than those in group 2( 1.79% , P <0.01 ).In addition, restenosis rates were significantly higher in group 1 than in group 2(41.18% vs 16.07%, P<0.05). Group 1 showed greater increases in left ventricular volume and less improvement in EF compared with group 2(ΔEDVI 6.31 ±2.17 vs 3.29 ±9.46ml/m 2 , ΔESVI 5.92 ±2.31 vs 3.86 ±1.08ml/m 2 , ΔEF 1.92 ±0.47 vs 4.79 ±1.73% , P <0.05 , respectively).Conclusions CRP levels within 6 hours after the onset of AMI might predict adverse outcome after primary PCI and progressive ventricular remodeling within 6 month of AMI.
文摘Objective To evaluate short time effects of primary percutaneous coronary intervention (pPCI) and rtPA thrombolysis+PCI (rtPA+PCI) on myocardial viability and ventricular systolic synchrony in AMI patients.Methods Eighty seven patients with first AMI were divided into two groups: group A ( n =42), pPCI group, the patients underwent PCI within 6h after onset of AMI; group B ( n =45), rtPA+PCI group, the patients underwent PCI after thrombolysis within 6h after onset of AMI; Myocardial viability was measured by 99m Tc MIBI SPECT. While, the parameters of cardiac function LVEF and ventricular systolic synchrony LVPS were measured by 99m Tc gated cardiac blood pool image on the first and the fourth weekend. Results (1) The peak CK MB was significantly lower in group A than that in group B( P <0.01 ). (2) Myocardial infarction area (MIA) was decreased and radioactivity counts in MIA was significantly increased in group A and B on the 4th weekend compared with that on the first weekend ( P <0.01 ), but there were no significant difference between group A and group B. (3) LVEF, LVPS were no significant difference between group A and group B.Conclusions (1)pPCI in acute myocardial infartion can limit infarct area, maintain ventricular systolic synchrony and improve ventricular function; (2) but, in those hospitals that there were no any condition for PCI, they should transfer the patients to central hospital for PCI after thrombolysis at the first time. It is beneficial to improve myocardial viability and ventricular systolic synchrony of AMI patients in short time.
文摘Objective Comparative study on the feasibility,safety and outcome of transradial artery and transfemoral artery access for primary percutaneous coronary intervention (PCI) in patients with acute myocardial infarction(AMI).Methods Two hundred and eight patients with AMI episoded within 12 hours, male 159, female 49, age 58.9 ±11.9 (34～88)years, were randomly divided into transradial artery access for primary PCI (TRA pPCI) group of 106 cases and transfemoral artery access for PCI (TFA pPCI) group of 102 cases during Sept, 2000 to Aug, 2002. The protocols of the manipulation duration and the effect for TRA pPCI and TFA pPCI procedures were respectively compared, including the time of transradial artery puncture and the rate of puncture success at first time ; the time of guiding catheter engaging into target coronary ostium; the rate of patence in infarct related artery (IRA); total duration of manipulation and the successful rate.The incidence of complications such as bleeding, vessel injury,thrombi and embolism as well as the average stay of hospitalization between two groups was compared. The status and the incidance of vessel spasm were observed and the effect of medicine administration to prevent from and relieve the vascular spasm was evaluated. The time of Allen’s test before and after TRA pPCI , the inner diameter and the peak of blood velocity of the right and left radial artery were investigated with color Doppler vessel echography as well as the complications of radial artery were followed up 1 month after TRA pPCI procedure. Results Two cases in every TRA pPCI and TFA pPCI groups were crossed over each other because procedure of the transradial or transfemoral access was failure. One handred and six vessels (48 vessels in LAD,22 vessels in LCX and 36 vessels in RCA) associated with 28 vessels of total occlusion in TRA pPCI group and 102 vessels (51 vessels in LAD,18 veesles in LCX and 33 vessels in RCA) with 24 vessels in total occlusion in TFA pPCI group were angioplasticized . The successful rates of the first time puncture in access artery, the re patence IRA and pPCI were similar in TRA pPCI and TFA pPCI groups ( 93.4% vs 96.1% ;100% vs 100%; 96.2% vs 97.1% , P >0.05 ). There were no significant diffierence in the average time of puncture time of access artery ,engaging in target vessels of guiding catheters and the total procedure of PCI between the two groups ( 1.3 ±0.3s vs 1.2 ±0.3s ; 6.0 ±1.6min vs 5.8 ±0.9min ; 49.2 ±24.1min vs 46.5 ± 26.4min , P >0.05 ). The access artery complications such as bleeding ,hematoma and embolism as well the veneous thrombosis in TFA pPCI group were much more than those in TRA pPCI group(p< 0.01 ). Although slight artery spasm of 4.7% cases in TRA pPCI group was happened during the procedure of PCI , the procedure had being continued after administration of medicine to release the spasm. The time of Allen’s test ,diameter and the systolic velocity of blood in daul radial arteries were no significant change before and after pPCI.Conclusions The duration and effect by TRA pPCI for AMI with stable hemodynamics was similar to TFA pPCI. The complications such as of bleeding,vessel injury, thrombi and embolism by TRA pPCI were few, and it was unnecessary to discontinue the anticoagulation medicine. TRA pPCI might be selected as a access vessel for pPCI in AMI patients with stable hemodynamics.
文摘Objective This study was to evaluate the efficacy and safety of a short acting reduced dose fibrinolytic regimen to promote early infarct related artery (IRA) patency for acyute myocardial infarction (AMI) patients referred for percutaneous coronary intervention (PCI).Methods Following aspirin and heparin, 166 patients were randomized to a 50 mg bolus of recombinant tissue type plasminogen activator(rt PA) or to a same volume sodium chloride injection followed by immediate primary PCI. The end points included patency rates on catheterization laboratory (cath lab) arrival, revascularization results when PCI was performed, complication rates, left ventricular function and restored patency rate following PCI. Results Patency on cath lab arrival was 64% with rt PA (34% TIMI 3,30% TIMI 2), while 31% of placebo (13% TIMI 3, 18% TIMI 2). There was no difference in the restored TIMI 3 rates of IRA between the two groups (85% vs 87%). No difference were observed in stroke or major bleeding. Left ventricular function was similar in both groups (52±9% vs 50±8%), but left ventricular ejection fraction fraction (LVEF) was higher with patent IRA (TIMI 3) on cath lab arrival than that of others (56±12% vs 48±10%).Conclusions Strategy thrombolytic regimens were compatible with subsequent PCI lead to more frequenc early recanalization (before cath lab arrival), which facilitates greater left ventricular function preservation with no augmentation of adverse events.
文摘Aim Salvia miltiorrhiza Bunge （SM） and lignum dalbergiae odoriferae （DO） are both traditional Chi- nese medicine that have cardioprotective effects. Here, we further examined the combined effects of SM and DO on rat myocardial ischemia/reperfusion injury. The possible mechanism of SM and DO also were elucidated. Methods DO was divided into aqueous extract of lignum dalbergiae odoriferae （DOW） and lignum dalbergiae odoriferae oil （DOO）. Sprague-Dawley rats were randomized to seven groups： sham group, model group, treatment groups inclu- ding SM （10 g · kg^-1）, DOW （5 g · kg^-1）, DOO （0.5 ml · kg^-1）, SM ＋ DOW （10 g · kg^-1 ＋ 5 g · kg^-1）, SM ＋ DOO （ 10 g · kg^-1 ＋ 0. 5 ml · kg^-1）. Rats were pretreated with homologous drug for 7 days and then subjec- ted to 30 rain of ischemia followed by 180 rain of reperfusion. Electrocardiogram （ECG） and heart rate were moni- tored and recorded continuously. At the end of reperfusion, blood samples were collected to determine the serum levels of creatine kinase-MB （CK-MB） and lactate dehydrogenase （LDH）. Hearts were harvested to assess heart- body rate, infarct size and histopathological changes as well. Maximum and minimum effective points were deter- mined by measuring indicators associate with myocardial injury at different time-points of reperfusion （Smin, 15min, 30min, 45rain, 60min, 120min, 180min）. The potential therapeutic mechanism of SM and SM ＋ DOO were carried out by detecting superoxide dismutase （SOD）, malondialdehyde （MDA）, tumor necrosis factor-alpha （TNF-alpha） and interleukin 6 （IL-6）. Results The results showed SM and DO can ameliorate cardiac function respectively, and this cardioprotective effect was further strengthened by their combinations. Among all the combi- nations, SM ＋ DOO showed predominant potential to improve ECG and heart rate, reduce heart-body rate （28.5% ＋ 1.4% , P 〈 0.01 vs model） and myocardial infarct size （ 20.96% ＋ 1.61% , P 〈 0.01 vs model, P 〈 0.05 vs SM） , attenuate histopathological damage, decrease the levels of CK-MB and LDH （P 〈 0.01 vs model, P 〈 0.05 vs SM）. The maximum effective points of SM and SM ＋ DOO were 15min and 30rain respectively, and the minimum effective points of them were 180rain. In reducing serum level of MDA, TNF-alpha, IL-6 and increasing SOD activ- ity, SM ＋ DOO was similar to SM. Conclusion The results of this study indicated that SM ＋ DOO have combined effects that are highly effective than single pretreatment against myocardial ischemie reperfusion injury in rats. The possible mechanism of SM and DO were likely through its anti-oxidant and anti-inflammatory properties, and thus may be an effective and promising medicine for both prophylaxis and treatment of ischemic heart disease.
基金The project supported by the Macao Science and Technology Development Fund(052/2013/A2)
文摘Erigeron multiradiatus(Lindl.)Benth.,has been used in Tibet folk medicine to treat various inflammatory diseases.The aim of this study was to investigate anti-myocardial ischemia and reperfusion(I/R)injury effect of caffeoylquinic acids derivatives of E.multiradiatus(AE)in vivo and to explain underling mechanism.AE was prepared using the whole plant of E.multiradiatus and contents of 6 caffeoylquinic acid determined through HPLC analysis.Myocardial I/R were induced by left anterior descending coronary artery occlusion for 30 min followed by 24 h of reperfusion in rats.AE administration(10,20 and 40 mg·kg-1)inhibited I/R-induced injury as indicated by decreasing myocardial infarct size,reducing of CK and LDH activities and preventing ST-segment depression in dose-dependent manner.AE decreased cardiac tissue levels of pro-inflammatory factors TNF-αand IL-6 and attenuated leukocytes infiltration.AE was further demonstrated to significantly inhibit I-κB degradation,nuclear translocation of p-65 and phosphorylation of JNK.Our results suggested that cardioprotective effect of AE could be due to suppressing myocardial inflammatory response and blocking NF-κB and JNK activation pathway.Thus,caffeoylquinic acids might be the active compounds in E.multiradiatus on myocardial ischemia and be a potential natural drug for treating myocardial I/R injury.
基金National Natural Science Foundation of China(81530100,81673802,81673712,81822049)。
文摘OBJECTIVE To investigate the effects of astragaloside IV(which can be extracted from the traditional Chinese medicine Astragalus membranaceus)on lipid and glucose metabolism in acute myocardial infarction(AMI).METHODS Model of heart failure(HF)after AMI was established with ligation of left anterior descending artery on Sprague-Dawley(SD)rats.The rats were divided into three groups:sham,model and astragaloside IV treatment group.Twenty-eight days after treatment(astragaloside IV,20 mg·kg-1 daily),hematoxylin-eosin(HE)staining was applied to visualize cardiomyocyte morphological changes.High performance liquid chromatography(HPLC)was performed to assess the contents of adenosine phosphates in heart.Positron emission tomography and computed tomography(PET-CT)was conducted to evaluate the cardiac glucose metabolism.Expressions of key molecules such as peroxisome proliferatoractivated receptor γ(PPARγ),sterol carrier protein 2(SCP2)and long chain acyl CoA dehydrogenase(ACADL)were measured by Western blotting and immunohistochemistry.Oxygen-glucose deprivation-reperfusion(OGD/R)-induced H9C2 injury cardiomyocyte model was adopted for potential mechanism research in vitro.RESULTS Treatment with astragaloside Ⅳ rescued hearts from structural and functional damages as well as inflammatory infiltration.Levels of adenosine triphosphate(ATP)and energy charge(EC)in astragaloside IV group were also up-regulated compared to model group.Further results demonstrated that critical enzymes both in lipid metabolism and glucose metabolism compro mised in model group compared to sham group.Intriguingly,astragalosideⅣcould up-regulate critical enzymes including ACADL and SCP2 in lipid metabolism accompanying with promoting effect on molecules in glycolysis simultaneously.Results on upstreaming signaling pathway demonstrated that astragaloside Ⅳ could dramatically increase the expres sions of PPARγ.In vitro study suggested the efficacy of astragalosideⅣcould be blocked by T0070907,a selective PPARγ inhibitor.CONCLUSION Astragaloside IV has cardioprotective effect in improving cardiac function and energy metabolism through regulating lipid and glucose metabolism.The effects may be mediated by PPARγ pathway.
基金Project(2012-0000478) supported by the National Research Foundation of Korea (NRF) grant funded by the Korea Government (MEST)
文摘In this work, we analyzed only the patients of the NSTEMI (non ST-segment elevation myocardial infarction) who arrived at the hospital within 12 h after symptoms started. Using NSTEMI follow-up data within, the characteristics of the clinical data, the risk factor, and the blood tested in the hospital visit were analyzed for MACE (major adverse cardiac events) patients. MACE includes cardiac death, MI (myocardial infarction), Re-PCI, and CABG (coronary artery bypass graft). As a result, from the NSTEMI patients which can be followed up for over 12 m, NT-ProBNP (p=0.014) and age (p=0.045) are found to be the independent risk factors related to MACE. Accordingly, they can be useful for the diagnosis and prognosis for NSTEMI patients as a biomarker.
文摘The YiQiFuMai powder injection （ YQFM）, a Traditional Chinese Medicine （TCM） prescription re-de- veloped based on the well-known TCM formula Sheng-maisan, showed a wide range of pharmacological activities in cardiovascular diseases in clinic. However, its role in protection against myocardial ischemia/reperfusion （MI/R） injury has not been elucidated. The present study not only evaluated the eardioprotective effect of YQFM from MI/ R injury but also investigated the potential molecular mechanisms in vivo and in vitro. The mouse model of MI/R injury was induced by a transient vessel occlusion for 30 rain and reperfusion for 24 h. The myocardium infarct size, production of lactate dehydrogenase （LDH）, creatine kinase （CK）, TUNEL staining and easpase-3 activity were measured. AMPKeα and phospho-AMPKα was analyzed by Western blot. We further verified the protective effect and potential molecular mechanisms of YQFM in an in vitro model of simulated ischemia and reperfusion （ SI/ R） in H9c2 cardiomyocytes. Cell viability was determined, and cell apoptosis were measured by Hoechst 33342 staining and Flow cytometry. Mitochondrial membrane potential （△ψFm） was measured, and ATP content was quantified by biolumineseent assay. Expression of apoptosis-related proteins including Caspase-3, Bcl-2, Bax, AMPKα and phospho-AMPKα was analyzed by Western blot. AMPKoL siRNA transfection was also applied to the mechanism elucidation. YQFM significantly reduced myocardium infarct size and the production of LDH, CK in se- rum, and also produced a significant decrease of apoptotic index which was confirmed by TUNEL staining and the changes of caspase-3 activity. In addition, pretreatment with YQFM markedly improved cell viability and decreased LDH release. Moreover, YQFM inhibited H9c2 apoptosis, blocked the expression of easpase-3 and modulated Bcl- 2 and Bax proteins, leading to an increased mitochondrial membrane potential and cellular ATP content. Mechanis- tically, YQFM activated AMPK signaling pathways while pretreatment with AMPK inhibitor compound C and appli- cation of transfection with AMPKα siRNA attenuated the anti-apoptotie effect of YQFM. Our results indicated that YQFM could provide significant cardioproteetion against MI/R injury, and potential mechanisms might to suppres- sion of cardiomyocytes apoptosis at least in part through activating the AMPK signaling pathways.
基金The project supported by the national scientific&technological major special project″significant creation of new drugs″(2013ZX09103001-008,2012ZX09103101-078,2013ZX09508104)
文摘OBJECTIVE To investigate the protective effect of salvianolic acid A(Sal A)on isoproterenol-induced myocardial infarction in mice and its possible mechanisms.METHODS The mice were subcutaneously injected with isopropranol(ISO 8mg·kg-1)to induce myocardial infarction and evaluated the myocardial protective effect of Sal A from mortality rate,electrocardiogram(ECG),heart function,myocardial infarction index,serum myocardial enzymes and explored its possible mechanisms from inflammatory,antioxidant and cells apoptosis.RESULTS Sal A can dose-dependently enhanced the heart function of myocardial infarction mice,reduced the heart index,inhibited the myocardial enzyme leakage,showed obvious myocardial protection effects.ELISA results showed that Sal A can reduce the expression of myocardial inflammatory cytokines such as IL-6,TNF-α.Western blotting confirmed that Sal A can increase the expression of anti-apoptotic proteins Bcl-2,reduce the expression of apoptosis protein Bax,and raise the phosphorylation level of PI3K and Akt.CONCLUSION Sal A have displayed significant protective effect against isoproterenol-induced myocardial infarction and its mechanism may be related to increasing of PI3K/Akt signal pathway and inhibition of cell apoptosis and inflammatory reaction.
文摘Aim Baroreflex dysfunction is associated with a higher rate of sudden death after myocardial infarction （MI）. Ketanserin enhances baroreflex function in rats. The present work was designed to examine whether ketan- serin improves the post-MI cardiac function and to explore the possible mechanism involved. Methods Spontane- ously hypertensive rats （SHR） were treated with ketanserin （0.3 mg · kg^-1 · d^-l）. Two weeks later, blood pres- sure and baroreflex function were measured, followed by a ligation of the left coronary artery. The expressions of ve- sicular acetylcholine transporter （VAChT） and α7 nicotinic acetylcholine receptor （α7-nAChR） in ischemic myo- cardium, angiogenesis, cardiac function, and left ventricular （LV） remodeling were evaluated subsequently. Re- sults Ketanserin significantly improved baroreflex sensitivity （0.62 ± 0. 21 vs. 0.34 ± 0. 12 ms/mmHg, P 〈 0.01 ） and vagal tonic activity （ heart rate changes in response to atropine, 54.8 ± 16.2 vs. 37.6 ± 13.4 b. p. m. , P 〈 0.01 ） without affecting the blood pressure or basic heart rate in SHR. Treatment of SHR with ketanserin promi- nently improved cardiac function and alleviated LV remodeling, as reflected by increases in the ejection fraction, fractional shortening, and LV systolic pressure as well as decreases in LV internal diameter and LV relative weight. The capillary density, vascular endothelial growth factor expression, and blood flow in the ischemic myocardium were significantly higher in the ketanserin-treated group. In addition, ketanserin markedly increased the expression of VAChT and α7-nAChR in ischemic myocardium. Conclusion Ketanserin improved post-MI cardiac function and angiogenesis in ischemic myocardium. The findings provide a mechanistic basis for restoring baroreflex function using ketanserin in the treatment of MI.
基金The project supported by National Natural Science Foundation of China(81573645,81603101,81473383)
文摘OBJECTIVE To investigate the protective effect of salvianolic acid A(Sal A)on isoproterenol-induced myocardial infarction in mice and its possible mechanisms.METHODS The mice were subcutaneously injected with isopropranol(ISO 8 mg·kg-1)to induce myocardial infarction and evaluated the myocardial protective effect of Sal A from mortality rate,electrocardiogram(ECG),heart function,myocardial infarction index,serum myocardial enzymes and explored its possible mechanisms from inflammatory,antioxidant and cells apoptosis.RESULTS Sal A can dose-dependently enhanced the heart function of myocardial infarction mice,reduced the heart index,inhibited the myocardial enzyme leakage,showed obvious myocardial protection effects.ELISA results showed that Sal A can reduce the expression of myocardial inflammatory cytokines such as IL-6,TNF-α.Western blotting confirmed that Sal A can increase the expression of anti-apoptotic proteins Bcl-2,reduce the expression of apoptosis protein Bax,and raise the phosphorylation level of PI3K and Akt.CONCLUSION Sal A have displayed significant protective effect against isoproterenol-induced myocardial infarction and its mechanism may be related to increasing of PI3K/Akt signal pathway and inhibition of cell apoptosis and inflammatory reaction.
基金Project supported by the Romanian National Authority for Scientific Research,CNCS-UEFISCDI,PNII(82/2012,194/2014)
文摘Myocardial infarction(MI)is a disorder that lowers the lifespan and quality of life.Reperfusion treatment as early as possible is the most effective solution,with an increased focus on post-MI medication.In the recovery process after MI,telocytes(TCs)appear to play an important role,which develops a large number of questions awaiting answers.Defining possible signaling mechanisms involved in recovery after MI may lead to identification the limits of current therapies,and development of new therapeutic solutions.Key words:telocytes;myocardial infarction;stem
文摘Objective To explore the variation of treatment and outcomes for NSTEMI across different-level hospitals, which potentially influenced by unbalanced economy and disparate medical care.Methods The China AMI registry consists of 108 hospitals across three levels (province, prefecture and county) throughout China.
文摘Background and Objective Elevated serum levels of lipoprotein(Lp[a]) has recently been proposed as a marker of cardiovascular risk.We aimed to determine the role of Lp(a) on long-term clinical outcomes in patients with ST elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI).
文摘OBJECTIVE To explore the potential molecular mechanism of Shenlian(SL)on myocardial ischemia(MI)on the basis of network pharmacology.METHODS Firstly,the main active ingredients of SL were screened in the Traditional Chinese Medicine Integrated Database,and the MI-associated targets were collected from the DisGeNET database.Then,we used compound-target and target-pathway networks to uncover the therapeutic mechanisms of SL On the basis of network pharmacology analysis results,we assessed the effects of SL in MI rat model and oxygen glu⁃cose deprivation model of H9c2 cells and validated the possible molecular mechanisms of SL on myocardial injury in vivo and in vitro.RESULTS The network pharmacology results showed that 37 potential targets were recognized,including TNF-α,Bcl-2,STAT3,PI3K,and MMP2.The pathways revealed that the possible targets of SL were involved in the reg⁃ulation of inflammation and apoptosis signaling pathway.Then,in vivo experiments indicated that SL significantly reduced the myocardial infarction size of MI rats.Serum CK-MB,cTnT,CK,LDH,and AST levels were significantly decreased by SL(P<0.05 or P<0.01).In vitro,SL significantly increased H9c2 cell viability.The levels of inflammation factors including TNF-αand MMP2 were significantly decreased by SL(P<0.05 or P<0.01).TUNEL and Annexin V/propidium iodide assays indicated that SL could significantly decrease the cell apoptotic rate in vivo and in vitro(P<0.05 or P<0.01).The remarkable upregulation of anti-apoptotic Bcl-2 and downregulation of pro-apoptotic Bax protein level further confirmed this result.Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that the PI3K-Akt and JAK2-STAT3 pathways were significantly enriched in SL.Compared with the model group,SL treatment significantly activated the PI3K-Akt and JAK2-STAT3 pathways in vivo and in vitro according to Western blotting analyses.CONCLU⁃SION SL could protect the myocardium from MI injury.The underlying mechanism may be related to the reduction of inflammation and apoptosis by activating the PI3K/Akt and JAK2/STAT3 pathways.
文摘Objective To assess the relationship of myocardial strain and torsion and quantitative heart function scores in patients with coronary heart disease after PTCA.Methods A total of 90 patients with coronary artery disease after PTCA were randomly divided into clinically normal heart function group(group A,n=43)and abnormal heart function group(group B,n=47),and 30 healthy people matched with age and gender as the control group(group C,n=30).
