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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 investigate the protective effect and mechanism of peroxisome proliferator-activated receptor-γ-coactivator-1α (PGC-1α) on oxygen-glucose deprived neurons. Methods: Seven days after primary culture, the cells were randomly divided into 4 groups: normal group, OGD group, OGD + PGC-1α overexpression plasmid group, OGD + Empty plasmid group (empty group). The overexpression group and the no-load group were pre-treated with PGC-1α overexpression plasmid and empty vector respectively before OGD treatment. The expression of PGC-1α was detected by Western blotting. The survival rate of neurons was detected by MTT assay and the content of reactive oxygen species (ROS) by flow cytometry. Results: The survival rate of neurons in OGD group was significantly lower than that in normal group (P <0.01). After PGC-1α overexpression plasmid was pretreated, the protein level of PGC-1α was significantly increased and the survival rate of neurons was increased. No-load group was significantly different (P <0.01). The level of ROS in neurons in OGD group was significantly higher than that in normal group (P <0.01). ROS level in OGD group was significantly lower than that in normal group (P <0.01). CONCLUSION: PGC-1α can significantly reduce the ROS content of neurons exposed to oxygen-glucose deprivation and improve its survival rate and exert its neuroprotective effects.