OBJECTIVE Shenfu injection(SFI)is an effective treatment of cardiogenic shock,the pathology of the central link was microcirculation disturbance.However,whether the microcirculation status of the early-and mid-stage o...OBJECTIVE Shenfu injection(SFI)is an effective treatment of cardiogenic shock,the pathology of the central link was microcirculation disturbance.However,whether the microcirculation status of the early-and mid-stage of cardiogenic shock has any difference is unclear.This study aimed to observe the effect of SFI on the microcirculatory disturbance in mesentery for early-and mid-stage of cardiogenic shock rat.METHODS The early-and mid-stage model of cardiogenic shock was established by ligating the ending or root of left anterior descending coronary arteries(LADCA).The rats were randomly divided into 9 groups,ie control group,early-stage model group,mid-stage model group,3 early medicated groups and 3 mid medicated groups(the dosage was 1,3.33,10 mL·kg^(-1) SFI for cardiogenic shock rats of early-and mid-stage,respectively).Parameters in mesenteric microcirculation,such as velocity of RBCs in venules,diameters of venules,the count of leukocyte adhesion and vascular permeability which calculated by FITC-dextran leakage were observed through an GeneandiM2 inverted intravital microscope and high-speed video camera system.RESULTS The cardiogenic shock induced by ligating the LADCA resulted in a number of responses in microcirculation,including a significant increase in the counts of adhesive leukocytes,narrowing of the vascular diameter,decrease in the velocity of RBCs and dextran efflux.All of the above parameters for early-stage cardiogenic shock rats were attenuated by the treatment with SFI,especially the dosage of 10 mL·kg^(-1).While SFI had no apparent time-effect on the vascular diameter and vascular permeability in mesentery for mid-stage cardiogenic shock rats.CONCLUSION The microcirculation status of the early-and mid-stage of cardiogenic shock rats were quite different.The efficacy of early treatment with SFI was more obvious than the mid administration,which could provide experimental and theoretical basis for the patients with cardiogenic shock in an earlier time.展开更多
OBJECTIVE To explore the biomarkers and molecular mechanism of Huanglianjiedu decoction(HJD) on high fat diet-induced experimental atherosclerosis in rats.METHODS SD male rats were randomly dividedinto five groups(n=8...OBJECTIVE To explore the biomarkers and molecular mechanism of Huanglianjiedu decoction(HJD) on high fat diet-induced experimental atherosclerosis in rats.METHODS SD male rats were randomly dividedinto five groups(n=8):normal control group,model group,and three dosage groups(1.5,3 and 6 g crude drug per kilogram of body weight).Atherosclerosis was induced by the combination of regular intraperitoneal injection of vitamin D3 and high fat diet for 8 weeks.HJD was administered by oral gavage from the third week once per day and until the end of the study.After the final administration,the blood samples were collected for biochemical analyses [total cholesterol(TC),triglycerides(TG),highdensity lipoprotein(HDL-C),low-density cholesterol(LDL-C)] and blood gas analyses(PaO_2,PaCO_2,pH,ctHb,etc);the abdominal aorta sections were stained with hematoxylin and eosin for histopathology;the liver homogenate were determined for MDA,SOD,OX-LDL,MCP-1 and VCAM-1.The plasma samples were detected using ultraper formance liquid chromatography coupled with quadrupole-time-of-flight tandem mass spectrometry(UPLC-Q-TOF-MS).The data of endogenous compounds were preliminarily preprocessed by software Progenesis QI and then analyzed by multivari.ate statistical analysis software EZinfo 2.0 to screen the distinguished biomarkers and the metabolic pathways were analyzed through website http://www.metaboanalyst.ca/.RESULTS Compared with the normal control group,the content of TC,TG,LDL-C,PaCO_2,MDA,Ox-LDL,MCP-1 and VCAM-1 were significantly increased and HDL-C,PaO_2,ctHb and SOD decreased in the atherosclerosis rats.HJD could significantly attenuated the high fat-induced atherosclerosis pathological injury and the abovementioned indexes(P<0.05).The five groups could be clearly distinguished using the metabolomics method.The administration groups profile exhibited an apparent returning trend from that of the model group and that of the normal control group.Twenty-one endogenous metabolites has been significantly changed in atherosclerosis rats.HJD could remarkably up-regulate 5-L-glutamyl-taurine,L-beta-aspartylL-glutamic acid,histidinyl-hydroxyproline,tryptophyl-alanine,4′-O-methyl-(-)-epicatechin,and downregulate protoporphyrin IX,azelaic acid,lacto-N-triaose,cinnamoylglycine and 9′-carboxy-alpha-tocotri.enol.CONCLUSION The beneficial effect of HJD in high fat-induced atherosclerosis rats may be due to anti-oxidant and anti-inflammatory.And it is suggested that HJD may affect the model rats through tryptophan metabolism,taurine and hypotaurine metabolism,histidine metabolism,lysine degradation and porphyrin and chlorophyll metabolism pathway.展开更多
基金supported by National Natural Science Foundation(2010CB530603)Science and Technology Development Plan of Lianyungang City(ZD1508)+1 种基金Natural Science Foundation of Jiangxi Province(20151BAB215037)Science and Technology Program of Health Department of Jiangxi Province(2015A039)
文摘OBJECTIVE Shenfu injection(SFI)is an effective treatment of cardiogenic shock,the pathology of the central link was microcirculation disturbance.However,whether the microcirculation status of the early-and mid-stage of cardiogenic shock has any difference is unclear.This study aimed to observe the effect of SFI on the microcirculatory disturbance in mesentery for early-and mid-stage of cardiogenic shock rat.METHODS The early-and mid-stage model of cardiogenic shock was established by ligating the ending or root of left anterior descending coronary arteries(LADCA).The rats were randomly divided into 9 groups,ie control group,early-stage model group,mid-stage model group,3 early medicated groups and 3 mid medicated groups(the dosage was 1,3.33,10 mL·kg^(-1) SFI for cardiogenic shock rats of early-and mid-stage,respectively).Parameters in mesenteric microcirculation,such as velocity of RBCs in venules,diameters of venules,the count of leukocyte adhesion and vascular permeability which calculated by FITC-dextran leakage were observed through an GeneandiM2 inverted intravital microscope and high-speed video camera system.RESULTS The cardiogenic shock induced by ligating the LADCA resulted in a number of responses in microcirculation,including a significant increase in the counts of adhesive leukocytes,narrowing of the vascular diameter,decrease in the velocity of RBCs and dextran efflux.All of the above parameters for early-stage cardiogenic shock rats were attenuated by the treatment with SFI,especially the dosage of 10 mL·kg^(-1).While SFI had no apparent time-effect on the vascular diameter and vascular permeability in mesentery for mid-stage cardiogenic shock rats.CONCLUSION The microcirculation status of the early-and mid-stage of cardiogenic shock rats were quite different.The efficacy of early treatment with SFI was more obvious than the mid administration,which could provide experimental and theoretical basis for the patients with cardiogenic shock in an earlier time.
基金supported by National Natural Science Foundation of China(8170382381560744) Science and Technology Research Project of Jiangxi Provincial Education Department(GJJ170753)
文摘OBJECTIVE To explore the biomarkers and molecular mechanism of Huanglianjiedu decoction(HJD) on high fat diet-induced experimental atherosclerosis in rats.METHODS SD male rats were randomly dividedinto five groups(n=8):normal control group,model group,and three dosage groups(1.5,3 and 6 g crude drug per kilogram of body weight).Atherosclerosis was induced by the combination of regular intraperitoneal injection of vitamin D3 and high fat diet for 8 weeks.HJD was administered by oral gavage from the third week once per day and until the end of the study.After the final administration,the blood samples were collected for biochemical analyses [total cholesterol(TC),triglycerides(TG),highdensity lipoprotein(HDL-C),low-density cholesterol(LDL-C)] and blood gas analyses(PaO_2,PaCO_2,pH,ctHb,etc);the abdominal aorta sections were stained with hematoxylin and eosin for histopathology;the liver homogenate were determined for MDA,SOD,OX-LDL,MCP-1 and VCAM-1.The plasma samples were detected using ultraper formance liquid chromatography coupled with quadrupole-time-of-flight tandem mass spectrometry(UPLC-Q-TOF-MS).The data of endogenous compounds were preliminarily preprocessed by software Progenesis QI and then analyzed by multivari.ate statistical analysis software EZinfo 2.0 to screen the distinguished biomarkers and the metabolic pathways were analyzed through website http://www.metaboanalyst.ca/.RESULTS Compared with the normal control group,the content of TC,TG,LDL-C,PaCO_2,MDA,Ox-LDL,MCP-1 and VCAM-1 were significantly increased and HDL-C,PaO_2,ctHb and SOD decreased in the atherosclerosis rats.HJD could significantly attenuated the high fat-induced atherosclerosis pathological injury and the abovementioned indexes(P<0.05).The five groups could be clearly distinguished using the metabolomics method.The administration groups profile exhibited an apparent returning trend from that of the model group and that of the normal control group.Twenty-one endogenous metabolites has been significantly changed in atherosclerosis rats.HJD could remarkably up-regulate 5-L-glutamyl-taurine,L-beta-aspartylL-glutamic acid,histidinyl-hydroxyproline,tryptophyl-alanine,4′-O-methyl-(-)-epicatechin,and downregulate protoporphyrin IX,azelaic acid,lacto-N-triaose,cinnamoylglycine and 9′-carboxy-alpha-tocotri.enol.CONCLUSION The beneficial effect of HJD in high fat-induced atherosclerosis rats may be due to anti-oxidant and anti-inflammatory.And it is suggested that HJD may affect the model rats through tryptophan metabolism,taurine and hypotaurine metabolism,histidine metabolism,lysine degradation and porphyrin and chlorophyll metabolism pathway.
