Apelin-13 inhibits apoptosis and excessive autophagy in cerebral ischemia/reperfusion injury

查看全文 作　　者：Zi-Qi [1]Shao;Shan-Shan [2]Dou;Jun-Ge [1]Zhu;Hui-Qing [1]Wang;Chun-Mei [2]Wang;Bao-Hua [2]Cheng;Bo [2]Bai

机构地区：[1]Cheeloo College of Medicine,Shandong University,Jinan,Shandong Province,China;[2]Neurobiology Institute,Jining Medical University,Jining,Shandong Province,China

出　　处：《Neural Regeneration Research》索引2021年第16卷第6期,共8页

基　　金：supported by the National Natural Science Foundation of China,Nos.81870948(to BB),81671276(to BHC),81501018(to CMW);the Natural Science Foundation of Shandong Province of China,No.ZR2014HL040(to BHC);Program Supporting Foundation for Teachers’Research of Jining Medical University of China,No.JYFC2018KJ003(to SSD). 摘　　要：Apelin-13 is a novel endogenous ligand for an angiotensin-like orphan G-protein coupled receptor,and it may be neuroprotective against cerebral ischemia injury.However,the precise mechanisms of the effects of apelin-13 remain to be elucidated.To investigate the effects of apelin-13 on apoptosis and autophagy in models of cerebral ischemia/reperfusion injury,a rat model was established by middle cerebral artery occlusion.Apelin-13(50μg/kg)was injected into the right ventricle as a treatment.In addition,an SH-SY5Y cell model was established by oxygen-glucose deprivation/reperfusion,with cells first cultured in sugar-free medium with 95%N2 and 5%CO2 for 4 hours and then cultured in a normal environment with sugar-containing medium for 5 hours.This SH-SY5Y cell model was treated with 10-7 M apelin-13 for 5 hours.Results showed that apelin-13 protected against cerebral ischemia/reperfusion injury.Apelin-13 treatment alleviated neuronal apoptosis by increasing the ratio of Bcl-2/Bax and significantly decreasing cleaved caspase-3 expression.In addition,apelin-13 significantly inhibited excessive autophagy by regulating the expression of LC3B,p62,and Beclin1.Furthermore,the expression of Bcl-2 and the phosphatidylinositol-3-kinase(PI3K)/Akt/mammalian target of rapamycin(mTOR)pathway was markedly increased.Both LY294002(20μM)and rapamycin(500 nM),which are inhibitors of the PI3K/Akt/mTOR pathway,significantly attenuated the inhibition of autophagy and apoptosis caused by apelin-13.In conclusion,the findings of the present study suggest that Bcl-2 upregulation and mTOR signaling pathway activation lead to the inhibition of apoptosis and excessive autophagy.These effects are involved in apelin-13-induced neuroprotection against cerebral ischemia/reperfusion injury,both in vivo and in vitro.The study was approved by the Animal Ethical and Welfare Committee of Jining Medical University,China(approval No.2018-JS-001)in February 2018. 关键词：central nervous system brain brain injury factor pathways apoptosis AUTOPHAGY NEUROPROTECTION regeneration

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Apelin-13 inhibits apoptosis and excessive autophagy in cerebral ischemia/reperfusion injury

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