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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 relationship between autophagy and apoptosis-induced TRAIL protein secretion in the process of astrocyte injury following cerebral ischemia. To mimic the ischemic environment, we employed both serum-deficient starvation environments to culture U251 and U87 both human glioma cells and examined the secretion of TRAIL protein and its effect on cell death. The results showed that the starvation environment can lead to autophagy and apoptosis of glial cells, and the process can be restored by nutrient supply. During the process of autophagy, the secretion of TRAIL protein also increased. The TRAIL protein indirectly induced by hunger-induced cell death was indirectly confirmed by TRAIL antibody blocking experiment. However, the regulatory mechanism of autophagy on TRAIL secretion, as well as the role of TRAIL in the autophagy and apoptosis regulatory networks, remains to be further experimental exploration.