Potentilla anserina polysaccharide alleviates cadmium-induced oxidative stress and apoptosis of H9c2 cells by regulating the MG53-mediated RISK pathway
作者机构:Institute of Integrated Traditional Chinese and Western MedicineSchool of Basic Medical SciencesLanzhou UniversityLanzhou 730000China School of NursingGansu University of Chinese MedicineLanzhou 730000China Key Laboratory of Dunhuang MedicineMinistry of EducationGansu University of Chinese MedicineLanzhou 730000China Institute of GeneticsSchool of Basic Medical SciencesLanzhou UniversityLanzhou 730000China Key laboratory of Evidence Science Techniques Research and Application of Gansu ProvinceGansu University of Political Science and LawLanzhou 730000China School of Basic Medical SciencesGansu University of Chinese MedicineLanzhou 730000China Department of Cardiac SurgeryThe First Hospital of Lanzhou UniversityLanzhou 730000China
出 版 物:《Chinese Journal of Natural Medicines》 (中国天然药物(英文版))
年 卷 期:2023年第21卷第4期
页 面:279-291页
核心收录:
学科分类:1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 100706[医学-药理学] 100602[医学-中西医结合临床] 10[医学]
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) 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)
主 题:Potentilla anserina L. Cadmium MG53 RISK pathway Oxidative stress Apoptosis Polysaccharide
摘 要:Oxidative stress plays a crucial role in cadmium(Cd)-induced myocardial *** 53(MG53)and its mediated reperfusion injury salvage kinase(RISK)pathway have been demonstrated to be closely related to myocardial oxidative *** anserina ***(PAP)is a polysaccharide with antioxidant capacity,which exerts protective effect on Cd-induced ***,it remains unknown whether PAP can prevent and treat Cd-induced cardiomyocyte *** present study was desgined to explore the effect of PAP on Cd-induced damage in H9c2 cells based on MG53 and the mediated RISK *** in vitro evaluation,cell viability and apoptosis rate were analyzed by CCK-8 assay and flow cytometry,***,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)*** mitochondrial function was measured by JC-10 staining and ATP detection *** blot was performed to detect the expression of proteins related to MG53,the RISK pathway,and *** results indicated that Cd increased the levels of reactive oxygen species(ROS)in H9c2 *** decreased the activities of SOD and CAT and the ratio of GSH/GSSG,resulting in decreases in cell viability and increases in ***,PAP reversed Cd-induced oxidative stress and cell ***,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/*** 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 ***,PAP alleviated Cd-induced MG53 reduction,activated the RISK pathway,and reduced mitochondrial dama