Oxidative stress plays a crucial role in cadmium(Cd)-induced myocardial injury.Mitsugumin 53(MG53)and its mediated reperfusion injury salvage kinase(RISK)pathway have been demonstrated to be closely related to myocard...Oxidative stress plays a crucial role in cadmium(Cd)-induced myocardial injury.Mitsugumin 53(MG53)and its mediated reperfusion injury salvage kinase(RISK)pathway have been demonstrated to be closely related to myocardial oxidative damage.Potentilla anserina L.polysaccharide(PAP)is a polysaccharide with antioxidant capacity,which exerts protective effect on Cd-induced damage.However,it remains unknown whether PAP can prevent and treat Cd-induced cardiomyocyte damages.The present study was desgined to explore the effect of PAP on Cd-induced damage in H9c2 cells based on MG53 and the mediated RISK pathway.For in vitro evaluation,cell viability and apoptosis rate were analyzed by CCK-8 assay and flow cytometry,respectively.Furthermore,oxidative stress was assessed by 2',7'-dichlorodihydrofluorescein diacetate(DCFH-DA)staining and using superoxide dismutase(SOD),catalase(CAT),and glutathione/oxidized glutathione(GSH/GSSG)kits.The mitochondrial function was measured by JC-10 staining and ATP detection assay.Western blot was performed to detect the expression of proteins related to MG53,the RISK pathway,and apoptosis.The results indicated that Cd increased the levels of reactive oxygen species(ROS)in H9c2 cells.Cd decreased the activities of SOD and CAT and the ratio of GSH/GSSG,resulting in decreases in cell viability and increases in apoptosis.Interestingly,PAP reversed Cd-induced oxidative stress and cell apoptosis.Meanwhile,Cd reduced the expression of MG53 in H9c2 clls and inhibited the RISK pathway,which was mediated by decreasing the ratio of p-Akt^(Ser473)/Akt,p-GSK3β^(Ser9)/GSK3β and p ERK1/2/ERK1/2.In addition,Cd impaired mitochondrial function,which involved a reduction in ATP content and mitochondrial membrane potential(MMP),and an increase in the ratio of Bax/Bcl-2,cytoplasmic cytochrome c/mitochondrial cytochrome c,and Cleaved-Caspase 3/Pro-Caspase 3.Importantly,PAP alleviated Cd-induced MG53 reduction,activated the RISK pathway,and reduced mitochondrial damage.Interestingly,knockdown of MG53 or inhibition of the RISK pathway attenuated the protective effect of PAP in Cd-induced H9c2 cells.In sum,PAP reduces Cd-induced damage in H9c2 cells,which is mediated by increasing MG53 expression and activating the RISK pathway.展开更多
文摘目的测定青藏高原4个主产地蕨麻的营养成分,并对其品质进行综合评价。方法采用SPSS 19.0分别对青藏高原4个主产地蕨麻的营养成分进行方差多重比较分析、主成分分析(principal component analysis,PCA)和聚类分析(hierarchical cluster analysis,HCA),并对蕨麻品质进行综合评价。结果4个不同主产地蕨麻中部分产地蕨麻的各营养成分之间差异显著(P<0.05),普遍具有高膳食纤维(平均含量>6 g/100 g)、低脂肪和低饱和脂肪(平均含量分别<3 g/100 g和<1.5 g/100 g)、极低钠(平均含量<40 mg/100 g)、氨基酸组成接近联合国粮食及农业组织和世界卫生组织(Food and Agriculture Organization of the United Nations/World Health Organization,FAO/WHO)的理想模式、脂肪酸种类丰富(含10种主要脂肪酸)、富含多种矿物质元素[平均Fe、Mg、K含量≥30%营养素参考值(nutrient reference values,NRV)]等特点。其中青海蕨麻为高蛋白食品(平均含量>20%NRV),四川和西藏蕨麻含有多种维生素(平均维生素B_(1)、维生素B_(2)、叶酸含量≥15%NRV)。PCA综合评价结果表明青海蕨麻排名第一,HCA将4个不同主产地蕨麻分为3类,第Ⅰ类蕨麻综合品质相对更好。结论蕨麻具有良好的营养价值和开发前景,青海蕨麻营养品质最佳,可为其质量控制提供依据。
基金supported by the Open Fund of Key Laboratory of Dunhuang Medicine,Ministry of Education(No.DHYX20-09)the Youth Research Foundation of Gansu University of Chinese Medicine(No.ZQ2017-14)+1 种基金the Natural Science Foundation of Gansu Province of China(No.20JR10RA600)the Young Doctors Fund Project of Colleges and Universities in Gansu Provine(No.2022QB-133)。
文摘Oxidative stress plays a crucial role in cadmium(Cd)-induced myocardial injury.Mitsugumin 53(MG53)and its mediated reperfusion injury salvage kinase(RISK)pathway have been demonstrated to be closely related to myocardial oxidative damage.Potentilla anserina L.polysaccharide(PAP)is a polysaccharide with antioxidant capacity,which exerts protective effect on Cd-induced damage.However,it remains unknown whether PAP can prevent and treat Cd-induced cardiomyocyte damages.The present study was desgined to explore the effect of PAP on Cd-induced damage in H9c2 cells based on MG53 and the mediated RISK pathway.For in vitro evaluation,cell viability and apoptosis rate were analyzed by CCK-8 assay and flow cytometry,respectively.Furthermore,oxidative stress was assessed by 2',7'-dichlorodihydrofluorescein diacetate(DCFH-DA)staining and using superoxide dismutase(SOD),catalase(CAT),and glutathione/oxidized glutathione(GSH/GSSG)kits.The mitochondrial function was measured by JC-10 staining and ATP detection assay.Western blot was performed to detect the expression of proteins related to MG53,the RISK pathway,and apoptosis.The results indicated that Cd increased the levels of reactive oxygen species(ROS)in H9c2 cells.Cd decreased the activities of SOD and CAT and the ratio of GSH/GSSG,resulting in decreases in cell viability and increases in apoptosis.Interestingly,PAP reversed Cd-induced oxidative stress and cell apoptosis.Meanwhile,Cd reduced the expression of MG53 in H9c2 clls and inhibited the RISK pathway,which was mediated by decreasing the ratio of p-Akt^(Ser473)/Akt,p-GSK3β^(Ser9)/GSK3β and p ERK1/2/ERK1/2.In addition,Cd impaired mitochondrial function,which involved a reduction in ATP content and mitochondrial membrane potential(MMP),and an increase in the ratio of Bax/Bcl-2,cytoplasmic cytochrome c/mitochondrial cytochrome c,and Cleaved-Caspase 3/Pro-Caspase 3.Importantly,PAP alleviated Cd-induced MG53 reduction,activated the RISK pathway,and reduced mitochondrial damage.Interestingly,knockdown of MG53 or inhibition of the RISK pathway attenuated the protective effect of PAP in Cd-induced H9c2 cells.In sum,PAP reduces Cd-induced damage in H9c2 cells,which is mediated by increasing MG53 expression and activating the RISK pathway.
