神经胶质细胞营养缺乏条件下引发细胞损伤效应分子机制研究

Molecular Mechanism of Glial Cell Damage Under the Cerebral Ischemia Environment

本文旨在探究脑缺血环境下,星形神经胶质细胞损伤过程中自噬与凋亡诱导TRAIL蛋白分泌的关系。为了模拟脑缺血的环境,我们采用培养基中血清缺乏的饥饿环境来培养U251和U87两种人脑神经胶质瘤细胞,并检测TRAIL蛋白的分泌及其对细胞死亡的作用。结果发现,饥饿环境可引发神经胶质细胞发生自噬和凋亡,且该过程可通过营养供给得到恢复。在细胞自噬过程中,TRAIL蛋白的分泌水平也得以升高,通过TRAIL蛋白抗体封闭实验间接证实了TRAIL蛋白对饥饿引发细胞死亡的促进作用。但自噬对TRAIL分泌的调控机理,以及TRAIL在细胞自噬和凋亡调控网络中的作用,还有待进一步的实验探究。

This article aims to explore the relation between autophagy and the protein secretion of TRAIL in the process of glial cell damage under the cerebral ischemia environment. In order to simulate the environment of cerebral ischemia, we intend to culture two species of human brain glioma cells, namely U251 and U87, with non-serum medium. And then detect the protein secretion of TRAIL and its role in cell death. In the experiment, we found that the secretion level of TRAIL protein has been improved in the process of autophagy under the starvation environment. By TRAIL＇s antibody blocking test on U87 and MTT assay, the promoting infl uence of TRAIL over autophagy has been indirectly testifi ed. However, the mechanism of autophagy＇s regulation of TRAIL secretion, as well as the simulation effectiveness of cerebral ischemia condition by starvation model, need further experimental exploration.