EGCG通过mTOR通路拮抗低氧诱导的PC12细胞的凋亡与自噬

发布时间：2018-04-23 08:29

本文选题：表没食子儿茶素没食子酸酯 + 雷帕霉素靶蛋白　；参考：《中国病理生理杂志》2014年11期

【摘要】：目的:氯化钴(cobalt chloride,Co Cl2)诱导的低氧具有神经毒性,可以诱导神经细胞的凋亡和自噬。茶多酚活性成分表没食子儿茶素没食子酸酯(epigallocatechin gallate,EGCG)具有一定的抗细胞凋亡和自噬的作用,但作用机理尚未完全阐明。近年来有研究报道,雷帕霉素靶蛋白(mammalian target of rapamycin,m TOR)通路参与了多种神经功能的调节,如神经细胞的分化成熟、抗氧化应激等。为此,我们用Co Cl2诱导低氧引起细胞的凋亡与自噬,从m TOR通路探讨EGCG拮抗Co Cl2诱导低氧引起细胞凋亡与自噬的作用机制。方法:研究使用Western blotting方法测定Co Cl2以及EGCG处理后m TOR和自噬蛋白beclin-1的表达,使用ELISA法检测细胞caspase-3表达,CCK-8检测细胞活力,免疫荧光法观察LC-3在胞核内的表达。结果:Co Cl2诱导低氧引起了细胞凋亡与自噬,而EGCG通过m TOR通路拮抗了Co Cl2诱导低氧引起的细胞凋亡与自噬,阻断m TOR通路则逆转了EGCG对神经细胞的保护作用。结论:EGCG通过m TOR通路拮抗了Co Cl2诱导的低氧引起的PC12细胞的凋亡与自噬。
[Abstract]:Aim: Cobalt chloridede Co Cl2) induced hypoxia-induced neurotoxicity, which can induce apoptosis and autophagy of nerve cells. Tea polyphenols active component epigallocatechin gallateEGCGG) has some anti-apoptosis and autophagy effects, but the mechanism has not been fully elucidated. In recent years, it has been reported that the rapamycin target protein mammalian target of rapamycin plays an important role in the regulation of neural function, such as neuronal differentiation and maturation, antioxidant stress and so on. Therefore, we used Co Cl2 to induce apoptosis and autophagy induced by hypoxia, and to explore the mechanism of EGCG antagonizing apoptosis and autophagy induced by Cl2 from m TOR pathway. Methods: Western blotting method was used to detect the expression of m TOR and autophagy beclin-1 after EGCG treatment, ELISA method was used to detect the expression of caspase-3 and CCK-8, and the expression of LC-3 in nucleus was detected by immunofluorescence. Results Cl2 induced apoptosis and autophagy induced by hypoxia, while EGCG antagonized apoptosis and autophagy induced by Cl2 via m TOR pathway. Blocking m TOR pathway reversed the protective effect of EGCG on neurons. ConclusionEGCG antagonizes apoptosis and autophagy of PC12 cells induced by Co Cl2 through m TOR pathway.
【作者单位】：南华大学附属第一医院;
【基金】：湖南省科技厅面上项目(No.2013FJ3133)
【分类号】：R363

【共引文献】