虫草多糖通过调控Nrf2/SLC7A11/GPX4信号通路改善神经元氧糖剥夺模型的氧化应激与铁死亡实验研究OA

Objective:To explore whether cordyceps polysaccharide(CSP)can improve the injury of neuronal oxygen-glucose deprivation(OGD)model by regulating nuclear factor E2-related factor 2(Nrf2)/solute carrier fami-ly 7 member 11(SLC7A11)/glutathione peroxidase 4(GPX4)signaling pathway.Methods:Human neuroblastoma cells SH-SY5Y were randomly divided into control group(CON group),model group(MOD group)and Cordyceps polysaccharide group(CSP group).OGD modeling was performed in CSP group after 24 hours pre-administration.Cell viability was measured by CCK-8 assay.The expression levels of glutathione peroxidase(GSH-Px),superoxide dismutase(SOD)and catalase(CAT)in SH-SY5Y cells were detected by corresponding kit.The expression levels of Nrf2,SLC7 A11,GPX4,long-chain fatty acyl-CoA synthetase 4(ACSL4),ferritin heavy chain 1(FTH1)and iron transporter 1(FPN1)in SH-SY5Y cells were detected by Western blot.Results:The cell viability of CSP group was significantly higher than that of MOD group(P＜0.05).The expression levels of GSH-Px,SOD,CAT,Nrf2,SLC7A11,GPX4,FTH1 and FPN1 in CSP group were higher than those in MOD group(all P＜0.05).The expres-sion of ACSL4 in CSP group was lower than that in MOD group(P＜0.05).Conclusion:CSP can regulate Nrf2/SLC7A11/GPX4 signaling pathway,promote the expression of antioxidant stress proteins and iron transporters in SH-SY5Y cells,and alleviate oxidative stress and ferroptosis damage caused by OGD model in SH-SY5Y cells.