文献类型：期刊文献

英文题名：Potentilla anserina polysaccharide alleviates cadmium-induced oxidative stress and apoptosis of H9c2 cells by regulating the MG53-mediated RISK pathway

作者：Zhao, Lixia[1,2,3];Cheng, Ju[4];Liu, Di[5];Gong, Hongxia[6];Bai, Decheng[1];Sun, Wei[7]

第一作者：Zhao, Lixia;赵丽霞

通信作者：Sun, W[1]

机构：[1]Lanzhou Univ, Inst Integrated Tradit Chinese & Western Med, Sch Basic Med Sci, Lanzhou 730000, Peoples R China;[2]Gansu Univ Chinese Med, Sch Nursing, Lanzhou 730000, Peoples R China;[3]Gansu Univ Chinese Med, Key Lab Dunhuang Med, Minist Educ, Lanzhou 730000, Peoples R China;[4]Lanzhou Univ, Inst Genet, Sch Basic Med Sci, Lanzhou 730000, Peoples R China;[5]Gansu Univ Polit Sci & Law, Key Lab Evidence Sci Tech Res & Applicat Gansu Pro, Lanzhou 730000, Peoples R China;[6]Gansu Univ Chinese Med, Sch Basic Med Sci, Lanzhou 730000, Peoples R China;[7]Lanzhou Univ, Hosp 1, Dept Cardiac Surg, Lanzhou 730000, Peoples R China

第一机构：Lanzhou Univ, Inst Integrated Tradit Chinese & Western Med, Sch Basic Med Sci, Lanzhou 730000, Peoples R China

通信机构：[1]corresponding author), Lanzhou Univ, Hosp 1, Dept Cardiac Surg, Lanzhou 730000, Peoples R China.

年份：2023

卷号：21

期号：4

起止页码：279

外文期刊名：CHINESE JOURNAL OF NATURAL MEDICINES

收录：;WOS:【SCI-EXPANDED(收录号:WOS:001007054600001)】；

基金：[Research funding] This work was 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 Founda-tion of Gansu Province of China (No. 20JR10RA600) , and the Young Doctors Fund Project of Colleges and Universities in Gansu Provine (No. 2022QB-133) .

语种：英文

外文关键词：Potentilla anserina L; Cadmium; MG53; RISK pathway; Oxidative stress; Apoptosis; Polysaccharide

摘要：Oxidative stress plays a crucial role in cadmium (Cd)-induced myocardial injury. Mitsugumin 53 (MG53) and its medi-ated 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-in-duced 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 path-way. For in vitro evaluation, cell viability and apoptosis rate were analyzed by CCK-8 assay and flow cytometry, respectively. Further-more, oxidative stress was assessed by 2 ',7 '-dichlorodihydrofluorescein diacetate (DCFH-DA) staining and using superoxide dis-mutase (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 de-creased 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 cells and inhibited the RISK pathway, which was mediated by decreasing the ratio of p-AktSer473/Akt, p-GSK3 beta Ser9/GSK3 beta 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 re-duced 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 ex-pression and activating the RISK pathway.