The Effect Of SIRT2 On Apoptosis And Mitochondrial Dynamics In Parkinson’s Disease Model Cells

Objective To investigate the effection and mechanism of cell apoptosis of si RNA knockdown silent information regulator 2(SIRT2)in Parkinson’s disease model cells induced by 1-methyl-4-phenylpyridinium(MPP~+).Methods Immortalized mouse hippocampal neuron HT22 cells was cultured in vitro and treated with MPP~+at different concentrations,and CCK-8 assay was used to detect cell inhibition.The cells were divided into control group,MPP~+optimal concentration group(1m M MPP~+treatment,injury group),the negative transfection group(based on the control group was transfected with SIRT2 negative sequence),the SIRT2-si RNA treatment group(based on the injury group was transfected with SIRT2-si RNA).The apoptosis of cells in each group was observed,apoptosis-related proteins(Bcl-2、Bax、Caspase-9)and the main proteins mediating fission and fusion of mitochondrial function(Drp1、Fis1、OPA1、Mfn1、Mfn2)were detected by Western blot.Results(1)When HT22 cells are treated at a concentration of 1m M MPP~+,the cell survival rate is about 55%,so this concentration is the best treatment concentration.(2)MPP~+induced increased expression of SIRT2 and increased apoptosis in the PD model constructed by HT22 cells.(3)Use si RNA to successfully down-regulate the expression of SIRT2 in the PD model.Western blot detects that the expression of apoptotic proteins(Bax,Caspase-9)decreases,and the expression of anti-apoptotic proteins(Bcl-2)increases.(4)Down-regulate the expression of SIRT2 in the PD model.Western blot showed that the expression of mitochondrial division proteins(Drp1,Fis1)decreased,and the expression of mitochondrial fusion proteins(Opa1,Mfn1,Mfn2)increased.Conclusion The expression of SIRT2 was significantly increased in a cell model of MPP-induced Parkinson’s disease,and inhibition the SIRT2 was able to decrease apoptosis,promote mitochondrial fusion,inhibit mitochondrial fission and protect neurons.