表食子儿茶素没食子酸酯对皮质酮损伤神经细胞的保护效应及其作用机制

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。

The effect of epigallocatechin gallate on corticosterone injured neurons and the involved mechanism

OBJECTIVE To investigate the effect of epigallocatechin gallate (EGCG) on corticosterone (CORT)-induced neurotoxicity and the important role of PI3K/Akt in the effect of EGCG.METHODS Injured PC12 cell model was established by 400 μmol·L^-1 CORT according to the cell viability detected by MTT assay. Change of cell morphology was observed by inverted microscope. Apotosis of cells was detected by Hochest stanining under the inverted microscope, and the relative expressions of p-Akt and Akt level was detected by Western blot analysis.RESULTS Compared with the control group, the cell viability decreased significantly, the cell shrunk remarkablly, the cell apotosis increased and the relative level of p-Akt also decreased in the CORT group. However, compared with the CORT group, the change of cell morphology was alleviated and the cell viability as well as the level of p-Akt/Akt were much higher. Furthermore, the effects of EGCG on cell morphology, cell viability, cell apotosis and p-Akt/Akt expression were inhibited by the PI3K/Akt inhibitor LY294002.CONCLUSION EGCG protects PC12 from CORT-induced neurotoxicity and PI3K/Akt signaling pathway plays a important role in the neuroprotective effects of EGCG.