APEX1 protects against oxidative damage-induced cardiomyocyte apoptosis

查看全文 作　　者：ZHAOHUI [1,2]HU;XIANGJUN [3]DING;YUYAO [2]JI;XIAOHONG [4]LIU;ZHIWEN [2]DING 机构地区：[1]Department of Cardiology,Tongji University Affiliated Tongji Hospital,Shanghai,200065,China;[2]Shanghai Institute of Cardiovascular Diseases,Zhongshan Hospital,Fudan University,Shanghai,200032,China;[3]The West Coast New Area of Qingdao Traditional Chinese Medicine Hospital,Qingdao,266500,China;[4]Cardiovascular Department of Internal Medicine,Central Hospital of Karamay,Karamay,834000,China 出　　处：《BIOCELL》索引2021年第45卷第3期,共5页 基　　金：supported by the National Natural Science Foundation of China(Grant No.81900245 and 81770395). 摘　　要：Apurine/pyrimidine-free endonuclease 1(APEX1)is a multifunctional enzyme that contributes to oxidization-mediated DNA-cleaved base excision repair and redox activation of transcription factors.However,the role of APEX1 during cardiomyocyte oxidative stress injury is not completely understood.In the present study,whether APEX1 protects oxidative damage-induced cardiomyocytes was investigated.mRNA and protein expression levels of APEX1 were downregulated in the mouse model of cardiac ischemia-reperfusion injury.Furthermore,the expression of APEX1 in hydrogen peroxide(H 2 O 2)-treated neonatal mice cardiomyocytes was also decreased.APEX1 knockdown aggravated H 2 O 2-treated cardiomyocyte apoptosis indexes.By contrast,APEX1 overexpression reversed H 2 O 2-induced oxidative damage,as demonstrated by decreased caspase 3 and Bax expression levels.Moreover,homeobox A5 upregulated APEX1.The results of the present study indicated that APEX1 displayed protective effects against oxidative damage,suggesting that APEX1 may serve as a unique protective strategy for cardiac ischemia-reperfusion injury. 关 键 词：Apurine/pyrimidine-free endonuclease 1 Cardiomyocyte apoptosis Cardiac ischemia-reperfusion