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目的:探讨过氧化物酶体增殖物激活受体-γ辅激活因子-lα(PGC-1α)对氧糖剥夺神经元的保护作用及机制.方法:原代培养胚胎小鼠大脑皮层神经元7 d,细胞随机分为4组:正常组、氧糖剥夺组(OGD组)、OGD+PGC-1α过表达质粒组(过表达组)、OGD+空载质粒组(空载组).过表达组与空载组分别于OGD处理前予以PGC-1α过表达质粒和空载质粒预处理.采用蛋白印迹技术检测PGC-1α表达,噻唑蓝比色分析(MTT)法检测神经细胞存活率,流式细胞仪检测活性氧(ROS)含量.结果:OGD组较正常组神经元存活率明显下降(P<0.01);予以PGC-1α过表达质粒预处理后,PGC-1α蛋白水平明显上调,其神经元存活率升高,与OGD组及空载组比较具有显著差异性(P<0.01).OGD组神经元ROS含量明显高于正常组(P<0.01);过表达组ROS水平降低,与OGD组及空载组ROS含量比较其差异具有统计学意义(P<0.01).结论:PGC-1α明显降低氧糖剥夺损伤神经元ROS含量,提高其生存率,发挥其神经保护作用.“,”Objective:To explore the protective effects and mechanism of Peroxisome proliferative activated receptor-γ activation of auxiliary factor 1 Alpha(PGC-1α) on injured neurons induced by oxygen-glucose deprivation(OGD) in embryonic mice.Methods: Cortical neurons cultured for 7 days were randomly divided into four groups:normal control group,oxygen-glucose deprivation group(OGD);OGD + PGC-1α overexpression plasmid group(overexpression group) and OGD +no-load plasmid group(no-loa d group).Overexpression group and the no-load group pretreatment with PGC-1α overexpression plasmid and no-load plasmid respectively before OGD treatment.24 hours after OGD,cell survival rate was detected by MTT(Methylthiazolyldiphenyl-tetrazolium bromide),observe the expression of PGC-1α was using Western blot technology,and the flow cytometry was used to monitor the content of Reactive Oxygen Species(ROS).Results:Compared with the normal control group,the cell survival rate in OGD group decreased(P<0.01),the survival rate was increased in overexpression group due to pretreatment of PGC-1α overexpression plasmid,which was compared with OGD group and no-load group with a significant difference(P<0.01).The ROS of OGD groups were significantly higher than that of the normal group(P<0.01);the content of ROS was decreased in overexpression group,and was significantly lower than that of the OGD group and no-load group(P<0.01).Conclusion:The study indicated that PGC-1α can significantly reduce the ROS content of oxygen-glucose deprivation neurons and improve its survival rate,to protect the neurons.