ANXA2通过抑制自死亡从而改善心肌细胞缺氧/复氧损伤的实验研究OA

Objective:Autosis,as a form of autophagy dependent cell death,plays a contradictory role in promoting survival and promoting death in myocardial ischemia-reperfusion injury(MIRI).The aim of this study was to investigate the effect of an-nexin A2(ANXA2)on MIRI and its mechanism by means of autosis.Methods:Cell hypoxia/reoxygenation(H/R)injury model was used to simulate MIRI,shRNA(shANXA2)targeting intervention was constructed,cell activity was detected by CCK-8,the ratio of autophagosome to autophagolysosome was observed by confocal microscopy,and autosis related protein expression was detected by Western blot.Results:The expression of ANXA2 was significantly increased in cardiomyocytes after H/R inju-ry,the expression of transcription factor EB(TFEB)was increased after downregulating ANXA2 expression,the proportion of autophagosomes was decreased,the proportion of lysosomes was increased,and cell viability was restored.Western blot results showed that down-regulation of ANXA2 decreased the levels of ANXA2,P62 and LC3II,and up-regulated the expression of TFEB.Conclusions:ANXA2 inhibits the expression of TFEB and nuclear translocation,affects autophagy flux and the occur-rence of autosis,and aggravates the H/R injury of cardiomyocytes.Down-regulation of ANXA2 promotes autophagy flux and re-duces the occurrence of autosis,thereby alleviating MIRI.This study provides experimental evidence for ANXA2 as a potential target for the treatment of MIRI.