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目的:研究表没食子儿茶素没食子酸酯(EGCG)对皮质酮损伤神经细胞的作用及对细胞内PI3K/Akt信号的影响。方法:用MTT法检测细胞损伤程度,构建皮质酮(CORT)应激损伤细胞模型;倒置显微镜下观察细胞形态变化;Hochest染色观察细胞凋亡情况;免疫印迹方法检测细胞p-Akt、Akt蛋白表达变化。结果:与正常对照组相比,模型组细胞存活率明显降低,细胞形态改变,突触收缩,凋亡增加,Akt磷酸化降低;当给予EGCG后,细胞存活率提高,细胞形态有所恢复,细胞凋亡减少,Akt磷酸化水平升高;先给予PI3K/Akt阻断剂后,EGCG对细胞存活率的升高作用和对细胞形态的缓解作用均被抑制。结论:EGCG能缓解CORT对PC12细胞的损伤作用,而PI3K/Akt信号在EGCG神经保护效应中具有重要作用。
AIM: To investigate the effect of epigallocatechin-3-gallate (EGCG) on cortical neurons injured by cortisone and its effect on PI3K / Akt signaling. Methods: The degree of cell injury was detected by MTT method. Cortical ketones (CORT) stress injury cell model was constructed. Morphological changes were observed under inverted microscope. Hochest staining was used to observe cell apoptosis. Western blotting was used to detect the expression of p-Akt and Akt Variety. Results: Compared with the normal control group, the survival rate of the model group was significantly decreased, the morphology of the cells was changed, the synaptic contraction and apoptosis were increased, and the phosphorylation of Akt was decreased. When EGCG was given, the cell survival rate was improved and the cell morphology recovered. Apoptosis decreased and Akt phosphorylation level increased. After PI3K / Akt blocker was administered, the effect of EGCG on cell survival and cell morphology was inhibited. Conclusion: EGCG can relieve the damage of CORT to PC12 cells, and PI3K / Akt signaling plays an important role in the neuroprotective effect of EGCG.