The secondary bud burst can cause around 10%-20%yield losses in black currants,an economically important crop in parts of Europe,Asia and North America.The metabolism of reactive oxygen species(ROS)has been linked to ...The secondary bud burst can cause around 10%-20%yield losses in black currants,an economically important crop in parts of Europe,Asia and North America.The metabolism of reactive oxygen species(ROS)has been linked to bud dormancy and its early release(secondary bud burst)in several fruit crops.But the relationship between ROS metabolism and the secondary bud burst is still not well understood in black currants.In the present study,two black currant cultivars(Adelinia and Heifeng)with opposing tendency of exhibiting the secondary bud burst were sprayed with abscisic acid(ABA)and gibberellic acid(GA_(3))to either inhibit or induce the secondary bud burst.The results showed that ABA inhibited the secondary bud burst by reducing the contents of ROS(H_(2)O_(2),O_(2)-·)in buds;decreasing the activities of superoxide dismutase(SOD),peroxidase(POD)and catalase(CAT);and increasing the contents of oxidized glutathione(GSSG)and ascorbic acid(AsA).GA_(3) effectively induced the secondary bud burst by increasing ROS contents;increasing the activities of several antioxidant enzymes,such as SOD,POD,CAT,glutathione reductase(GR),ascorbate peroxidase(APX)and the contents of reduced glutathione(GSH);and decreasing the contents of AsA.The experimental results showed that GA_(3) treatment increased the content of ROS,accelerated the metabolism of reactive oxygen species,and promoted the second burst of black currants.However,ROS metabolism was at a low level under ABA treatment,and the buds remained dormant.These results suggested that ROS metabolism might play an important role in the two black currants of the secondary bud burst.展开更多
AIM:To explore the influence of ethyl(2,4,6-trimethylbenzoyl)phenylphosphinate(TPOL)on cell apoptosis and its potential mechanism.METHODS:HEK293T cells sensitive to TPOL were treated with different concentrations of T...AIM:To explore the influence of ethyl(2,4,6-trimethylbenzoyl)phenylphosphinate(TPOL)on cell apoptosis and its potential mechanism.METHODS:HEK293T cells sensitive to TPOL were treated with different concentrations of TPOL with or without exposure to light radiation,before treatment with various inhibitors,N-acetyl-Lcysteine(NAC),pifithrin-αand Z-DVED-FMK.Cell viability was measured by CCK-8 assay.Annexin V/propidium iodide staining was used to count the number of apoptotic cells.DCFH-DA staining was used to detect reactive oxygen species(ROS)levels,and JC-1 staining was used to assess mitochondrial membrane potential by flow cytometry.The expression of apoptosis-related proteins and cell cycle-regulated molecules was measured by Western blot.RESULTS:TPOL enhanced the apoptosis of HEK293T cells in a dose-dependent manner(P<0.05),with a decrease in Bcl-2 and increases in Bax and cytochrome C(Cyto C),followed by up-regulation of activated caspase-9 and caspase-3,and the cleavage of PARP(P<0.05).The TPOL-enhanced cleavage of caspase-3 and PARP was rescued by Z-DVED-FMK(P<0.01).TPOL also led to a rapid increase in ROS,a reduction in mitochondrial membrane potential,and the release of Cyto C(P<0.01),all of which could be reversed by the ROS scavenger NAC.Moreover,the TPOL-caused alterations in p21,p27,Rb,and CDK2 were also recovered by the p53 inhibitor pifithrin-α(P<0.05).The TPOL-induced changes in Bax,Bcl-2,cleaved caspase-9,activated caspase-3,and cleaved PARP were subsequently rescued by pretreatment with pifithrin-α(P<0.05).CONCLUSION:TPOL can induce cellular apoptosis with ROS-mediated mitochondrial membrane damage through the activation of a ROS-dependent p53/p21/p27/Rb/Bax/Cyto C/caspase-mediated signal axis.展开更多
Salt stress is a major abiotic stress limiting plant growth and yield. In the present study, the effects of exogenous H_(2)O_(2) on the reactive oxygen species(ROS) metabolism and the antioxidant system in leaves of N...Salt stress is a major abiotic stress limiting plant growth and yield. In the present study, the effects of exogenous H_(2)O_(2) on the reactive oxygen species(ROS) metabolism and the antioxidant system in leaves of Nitralia tangutorum Bobr. under salt stress were studied. N. tangutorum seedlings were subjected to 200 mmol·L^(-1) NaCl treatment with or without the exogenous application of H_(2)O_(2) for 7 days. The results showed that NaCl stress significantly increased the relative conductivity, the contents of thiobarbituric acid reactive substances(TBARS) and ROS(H_(2)O_(2) and O_(2)^(·-)), as well as promoted the activities of antioxidant enzymes including superoxide dismutase(SOD), peroxidase(POD), catalase(CAT), and ascorbate peroxidase(APX) in N. tangutorum leaves. In addition, exogenous H_(2)O_(2) decreased the relative conductivity, the contents of TBARS, H_(2)O_(2) and O_(2)^(·-), while further enhanced the activities of antioxidant enzymes. These results indicated that H_(2)O_(2) effectively alleviated the adverse effects of NaCl stress on N. tangutorum through the regulation of ROS metabolism.展开更多
Oxidative stress occurs when crop plants are exposed to extreme abiotic conditions that lead to the excessive production and accumulation of reactive oxygen species(ROS).Those extreme abiotic conditions or stresses in...Oxidative stress occurs when crop plants are exposed to extreme abiotic conditions that lead to the excessive production and accumulation of reactive oxygen species(ROS).Those extreme abiotic conditions or stresses include drought,high temperature,heavy metals,salinity,and ultraviolet radiation,and they cause yield and quality losses in crops.ROS are highly reactive species found in nature that can attack plant organelles,metabolites,and molecules by interrupting various metabolic pathways until cell death occurs.Plants have evolved defense mechanisms for the production of antioxidants to detoxify the ROS and to protect the plant against oxidative damage.Modern researches in crop plants revealed that low levels of ROS act as a signal which induces tolerance to environmental extremes by altering the expression of defensive genes.In this review,we summarized the processes involved in ROS production in response to several types of abiotic stress in cotton plants.Furthermore,we discussed the achievements in the understanding and improving oxidative stress tolerance in cotton in recent years.Researches related to plant oxidative stresses have shown excellent potential for the development of stress-tolerant crops.展开更多
OBJECTIVE To investigates the effects of imperatorin on the oxidative stress in the cerebral cortex and hippocampus after focal cerebral ischemia/reperfusion injury.METHODS Transient focal cerebral ischemia/reperfusio...OBJECTIVE To investigates the effects of imperatorin on the oxidative stress in the cerebral cortex and hippocampus after focal cerebral ischemia/reperfusion injury.METHODS Transient focal cerebral ischemia/reperfusion model in male Sprague-Dawley rats was induced by 2 h middle cerebral artery occlusion followed by 24 h reperfusion.Imperatorin(1.25 and 2.5 mg·kg-1)or vehicle were administered intraperitoneally at 1,5 and 9 h after the onset of ischemia.At 24 h after reperfusion,the biomarkers of oxidative stress such as the levels of reactive oxygen species(ROS),lipid peroxidation products malondialdehyde(MDA),nitric oxide(NO)and total antioxidant capacity(T-AOC),the activities of inducible nitric oxide synthase(iN OS),superoxide dismutase(SOD)and catalase(CAT)in the cerebral cortex and hippocampus were observed.We also assessed the nuclear factor erythroid 2-related factor 2(Nrf2),heme oxygenase-1(HO-1),and the NAD(P)H-quinone oxidoreductase 1(NQO-1)protein expression by Western blot.RESULTS As compared to vehicle-treated animals,imperatorin treatment significantly reduced the ROS,MDA,NO levels and i NOS activity,increased T-AOC and the activities of SOD and CAT.Furthermore,imperatorin treatment also significantly induced the nuclear translocation of Nrf2,enhanced the protein expression of HO-1 and NQO-1 in the cerebral cortex and hippocampus.CONCLUSION Our findings indicate that imperatorin can protect the brain against the excessive oxidative stress induced by cerebral ischemia/reperfusion through activation of Nrf2 signaling pathway.展开更多
The purpose of this study was to explore the effects of recombinant human intestinal alkaline phosphatase(recIAP) on human neutrophils in vitro, and the migration, phagocytosis, apoptosis in presence and absence of LP...The purpose of this study was to explore the effects of recombinant human intestinal alkaline phosphatase(recIAP) on human neutrophils in vitro, and the migration, phagocytosis, apoptosis in presence and absence of LPS. In this study, freshly extracted human neutrophils were used to establish an inflammatory cell model, and the control group, recIAP group, LPS group and recIAP +LPS group were set up to stimulate the model. The migration of neutrophils was detected by agarose gel drop method. Fluorescent particles and fluorescent probes were added to different treatment groups, and the phagocytic rate of neutrophils and the release of reactive oxygen species(ROS) from neutrophils were detected by flow cytometry. The apoptosis rate of neutrophils was detected by flow cytometry according to Annexin V-FITC apoptosis detection kit. The results showed that regardless of the presence or absence of LPS, recIAP could inhibit the migration of neutrophils, phagocytosis and the release of ROS. In addition, recIAP could weaken the inhibitory effect of LPS on neutrophils apoptosis.展开更多
OBJECTIVE In order to investigate the possible anti-tumor molecular mechanisms of gecko polypeptide mixture(GPM).METHODS RNA-seq technology was used to identify the differentially expressed genes of human hepatocellul...OBJECTIVE In order to investigate the possible anti-tumor molecular mechanisms of gecko polypeptide mixture(GPM).METHODS RNA-seq technology was used to identify the differentially expressed genes of human hepatocellular carcinoma(HCC)HepG2 cells treated with or without GPM.The HepG2 cells were treated with different concentration of GPM(0,0.1,0.2,0.3,0.4 mg·mL^(-1))for 6 h,12 h and 24 h,respectively.MTT assay was used to detect the viability of HepG2 cells.DAPI fluorescence staining was performed to observe nucleus morphological changes of HepG2 cells.Western blot analysis was applied to observe the expression of apoptosis-related proteins in HepG2 cells.RESULTS The results showed that GPM could induce HepG2 cells apoptosis and influence HepG2 cells proliferation in a dose-dependent manner.We applied many analysis methods,including differentially expressed genes analysis,Gene Ontology(GO)enrichment analysis,KEGG pathway enrichment analysis,protein-protein interaction network analysis to screen out possible molecular mechanisms.ER-nucleus signaling pathway,cellular response to stress and apoptotic processes were identified the potential anti-cancer molecular biological process of GPM.GPM may also induce apoptosis in HepG2 cells via endoplasmic reticulum stress pathway.The mechanism is closely related to ERs,which might be beneficial for clinical therapy of HCC.CONCLUSION GPM can inhibit cells proliferation and induce apoptosis in HepG2 cells.The gene expression profile of GPM in HepG2 cells was obtained.The present study revealed the potential anti-tumor mechanism of GPM.展开更多
基金Supported by Academic Backbone Project of Northeast Agricultural University(20XG04)the National Key R&D Program of China(2018YFD1000200)Heilongjiang Province Postdoctoral Startup Fund(LBH-Q17029)。
文摘The secondary bud burst can cause around 10%-20%yield losses in black currants,an economically important crop in parts of Europe,Asia and North America.The metabolism of reactive oxygen species(ROS)has been linked to bud dormancy and its early release(secondary bud burst)in several fruit crops.But the relationship between ROS metabolism and the secondary bud burst is still not well understood in black currants.In the present study,two black currant cultivars(Adelinia and Heifeng)with opposing tendency of exhibiting the secondary bud burst were sprayed with abscisic acid(ABA)and gibberellic acid(GA_(3))to either inhibit or induce the secondary bud burst.The results showed that ABA inhibited the secondary bud burst by reducing the contents of ROS(H_(2)O_(2),O_(2)-·)in buds;decreasing the activities of superoxide dismutase(SOD),peroxidase(POD)and catalase(CAT);and increasing the contents of oxidized glutathione(GSSG)and ascorbic acid(AsA).GA_(3) effectively induced the secondary bud burst by increasing ROS contents;increasing the activities of several antioxidant enzymes,such as SOD,POD,CAT,glutathione reductase(GR),ascorbate peroxidase(APX)and the contents of reduced glutathione(GSH);and decreasing the contents of AsA.The experimental results showed that GA_(3) treatment increased the content of ROS,accelerated the metabolism of reactive oxygen species,and promoted the second burst of black currants.However,ROS metabolism was at a low level under ABA treatment,and the buds remained dormant.These results suggested that ROS metabolism might play an important role in the two black currants of the secondary bud burst.
基金Supported by the National Natural Science Foundation of China(No.81172824)。
文摘AIM:To explore the influence of ethyl(2,4,6-trimethylbenzoyl)phenylphosphinate(TPOL)on cell apoptosis and its potential mechanism.METHODS:HEK293T cells sensitive to TPOL were treated with different concentrations of TPOL with or without exposure to light radiation,before treatment with various inhibitors,N-acetyl-Lcysteine(NAC),pifithrin-αand Z-DVED-FMK.Cell viability was measured by CCK-8 assay.Annexin V/propidium iodide staining was used to count the number of apoptotic cells.DCFH-DA staining was used to detect reactive oxygen species(ROS)levels,and JC-1 staining was used to assess mitochondrial membrane potential by flow cytometry.The expression of apoptosis-related proteins and cell cycle-regulated molecules was measured by Western blot.RESULTS:TPOL enhanced the apoptosis of HEK293T cells in a dose-dependent manner(P<0.05),with a decrease in Bcl-2 and increases in Bax and cytochrome C(Cyto C),followed by up-regulation of activated caspase-9 and caspase-3,and the cleavage of PARP(P<0.05).The TPOL-enhanced cleavage of caspase-3 and PARP was rescued by Z-DVED-FMK(P<0.01).TPOL also led to a rapid increase in ROS,a reduction in mitochondrial membrane potential,and the release of Cyto C(P<0.01),all of which could be reversed by the ROS scavenger NAC.Moreover,the TPOL-caused alterations in p21,p27,Rb,and CDK2 were also recovered by the p53 inhibitor pifithrin-α(P<0.05).The TPOL-induced changes in Bax,Bcl-2,cleaved caspase-9,activated caspase-3,and cleaved PARP were subsequently rescued by pretreatment with pifithrin-α(P<0.05).CONCLUSION:TPOL can induce cellular apoptosis with ROS-mediated mitochondrial membrane damage through the activation of a ROS-dependent p53/p21/p27/Rb/Bax/Cyto C/caspase-mediated signal axis.
基金Supported by the Natural Science Foundation of Heilongjiang Province(LH2019C021)。
文摘Salt stress is a major abiotic stress limiting plant growth and yield. In the present study, the effects of exogenous H_(2)O_(2) on the reactive oxygen species(ROS) metabolism and the antioxidant system in leaves of Nitralia tangutorum Bobr. under salt stress were studied. N. tangutorum seedlings were subjected to 200 mmol·L^(-1) NaCl treatment with or without the exogenous application of H_(2)O_(2) for 7 days. The results showed that NaCl stress significantly increased the relative conductivity, the contents of thiobarbituric acid reactive substances(TBARS) and ROS(H_(2)O_(2) and O_(2)^(·-)), as well as promoted the activities of antioxidant enzymes including superoxide dismutase(SOD), peroxidase(POD), catalase(CAT), and ascorbate peroxidase(APX) in N. tangutorum leaves. In addition, exogenous H_(2)O_(2) decreased the relative conductivity, the contents of TBARS, H_(2)O_(2) and O_(2)^(·-), while further enhanced the activities of antioxidant enzymes. These results indicated that H_(2)O_(2) effectively alleviated the adverse effects of NaCl stress on N. tangutorum through the regulation of ROS metabolism.
文摘Oxidative stress occurs when crop plants are exposed to extreme abiotic conditions that lead to the excessive production and accumulation of reactive oxygen species(ROS).Those extreme abiotic conditions or stresses include drought,high temperature,heavy metals,salinity,and ultraviolet radiation,and they cause yield and quality losses in crops.ROS are highly reactive species found in nature that can attack plant organelles,metabolites,and molecules by interrupting various metabolic pathways until cell death occurs.Plants have evolved defense mechanisms for the production of antioxidants to detoxify the ROS and to protect the plant against oxidative damage.Modern researches in crop plants revealed that low levels of ROS act as a signal which induces tolerance to environmental extremes by altering the expression of defensive genes.In this review,we summarized the processes involved in ROS production in response to several types of abiotic stress in cotton plants.Furthermore,we discussed the achievements in the understanding and improving oxidative stress tolerance in cotton in recent years.Researches related to plant oxidative stresses have shown excellent potential for the development of stress-tolerant crops.
基金supported by National Natural Science Foundation of China(81060269 and81360492)Natural Science Foundation of Jiangxi Province of China(20122BAB205036)
文摘OBJECTIVE To investigates the effects of imperatorin on the oxidative stress in the cerebral cortex and hippocampus after focal cerebral ischemia/reperfusion injury.METHODS Transient focal cerebral ischemia/reperfusion model in male Sprague-Dawley rats was induced by 2 h middle cerebral artery occlusion followed by 24 h reperfusion.Imperatorin(1.25 and 2.5 mg·kg-1)or vehicle were administered intraperitoneally at 1,5 and 9 h after the onset of ischemia.At 24 h after reperfusion,the biomarkers of oxidative stress such as the levels of reactive oxygen species(ROS),lipid peroxidation products malondialdehyde(MDA),nitric oxide(NO)and total antioxidant capacity(T-AOC),the activities of inducible nitric oxide synthase(iN OS),superoxide dismutase(SOD)and catalase(CAT)in the cerebral cortex and hippocampus were observed.We also assessed the nuclear factor erythroid 2-related factor 2(Nrf2),heme oxygenase-1(HO-1),and the NAD(P)H-quinone oxidoreductase 1(NQO-1)protein expression by Western blot.RESULTS As compared to vehicle-treated animals,imperatorin treatment significantly reduced the ROS,MDA,NO levels and i NOS activity,increased T-AOC and the activities of SOD and CAT.Furthermore,imperatorin treatment also significantly induced the nuclear translocation of Nrf2,enhanced the protein expression of HO-1 and NQO-1 in the cerebral cortex and hippocampus.CONCLUSION Our findings indicate that imperatorin can protect the brain against the excessive oxidative stress induced by cerebral ischemia/reperfusion through activation of Nrf2 signaling pathway.
基金the Heilongjiang Natural Science Fund Project (C2017035)。
文摘The purpose of this study was to explore the effects of recombinant human intestinal alkaline phosphatase(recIAP) on human neutrophils in vitro, and the migration, phagocytosis, apoptosis in presence and absence of LPS. In this study, freshly extracted human neutrophils were used to establish an inflammatory cell model, and the control group, recIAP group, LPS group and recIAP +LPS group were set up to stimulate the model. The migration of neutrophils was detected by agarose gel drop method. Fluorescent particles and fluorescent probes were added to different treatment groups, and the phagocytic rate of neutrophils and the release of reactive oxygen species(ROS) from neutrophils were detected by flow cytometry. The apoptosis rate of neutrophils was detected by flow cytometry according to Annexin V-FITC apoptosis detection kit. The results showed that regardless of the presence or absence of LPS, recIAP could inhibit the migration of neutrophils, phagocytosis and the release of ROS. In addition, recIAP could weaken the inhibitory effect of LPS on neutrophils apoptosis.
基金supported by Science and Technology Key Research Fund of Henan Province(142102310031)
文摘OBJECTIVE In order to investigate the possible anti-tumor molecular mechanisms of gecko polypeptide mixture(GPM).METHODS RNA-seq technology was used to identify the differentially expressed genes of human hepatocellular carcinoma(HCC)HepG2 cells treated with or without GPM.The HepG2 cells were treated with different concentration of GPM(0,0.1,0.2,0.3,0.4 mg·mL^(-1))for 6 h,12 h and 24 h,respectively.MTT assay was used to detect the viability of HepG2 cells.DAPI fluorescence staining was performed to observe nucleus morphological changes of HepG2 cells.Western blot analysis was applied to observe the expression of apoptosis-related proteins in HepG2 cells.RESULTS The results showed that GPM could induce HepG2 cells apoptosis and influence HepG2 cells proliferation in a dose-dependent manner.We applied many analysis methods,including differentially expressed genes analysis,Gene Ontology(GO)enrichment analysis,KEGG pathway enrichment analysis,protein-protein interaction network analysis to screen out possible molecular mechanisms.ER-nucleus signaling pathway,cellular response to stress and apoptotic processes were identified the potential anti-cancer molecular biological process of GPM.GPM may also induce apoptosis in HepG2 cells via endoplasmic reticulum stress pathway.The mechanism is closely related to ERs,which might be beneficial for clinical therapy of HCC.CONCLUSION GPM can inhibit cells proliferation and induce apoptosis in HepG2 cells.The gene expression profile of GPM in HepG2 cells was obtained.The present study revealed the potential anti-tumor mechanism of GPM.
