人神经干细胞微囊泡对谷氨酸诱导PC12细胞损伤的保护作用

目的: 探究人神经干细胞微囊泡(human neural stem cell microvesicles, hNSC-MVs)对谷氨酸诱导PC12细胞损伤的作用及可能机制。方法: 采用谷氨酸处理大鼠肾上腺髓质嗜铬细胞瘤PC12细胞，建立兴奋性损伤模型；实验分为3组：对照组，PC12细胞未经任何处理；谷氨酸组，谷氨酸处理PC12细胞24 h；hNSC-MVs+谷氨酸组，200 mg/L hNSC-MVs预处理PC12细胞24 h，再加入谷氨酸处理24 h。MTT法检测各组PC12细胞存活率；免疫印迹实验检测细胞凋亡相关蛋白Bax和Bcl-2表达。结果： PC12细胞能内化hNSC-MVs。谷氨酸对PC12细胞具有毒性作用，其半数抑制浓度为25 mmol/L。与谷氨酸组相比，hNSC-MVs+谷氨酸组PC12细胞存活率明显增高(P<0.01)。与对照组相比，谷氨酸组Bax蛋白表达显著升高，Bcl-2蛋白表达显著降低，而与谷氨酸组相比，hNSC-MVs+谷氨酸组Bax蛋白表达明显下调，Bcl-2蛋白表达明显上调(P均<0.01)。结论： hNSC-MVs可能通过抑制谷氨酸诱导的PC12细胞凋亡，从而发挥保护作用。

Protective effect of human neural stem cell microvesicles against glutamate induced cytotoxicity in PC12 cells

Objective: To investigate the effect of human neural stem cell microvesicles (hNSC MVs) against glutamate-induced cytotoxicity in PC12 cells and its possible mechanism. Methods: Excitative injury model was established by treating rat adrenal medulla pheochromocytoma PC12 cells with glutamate. Experiment was divided into three groups: control group, PC12 cells without any treatment; glutamate group, PC12 cells treated with glutamate for 24 h; hNSC-MVs + glutamate group, PC12 cells were pretreated with 200 mg/L hNSC-MVs for 24 h, and then treated with glutamate for 24 h. MTT method was used to detect the survival rate of PC12 cells and Western blotting was used to determine the expression of apoptosis-related proteins, Bax and Bcl-2. Results: PC12 cells could internalize hNSC-MVs. Glutamate has a toxic effect on PC12 cells, and its half inhibitory concentration is 25 mmol/L. Compared with glutamate group, the survival rate of PC12 cells in hNSC-MVs + glutamate group was surprisingly increased(P<0.01). Compared with control group, the expression of Bax protein in glutamate group was markedly increased, and the expression of Bcl-2 protein was greatly reduced. Compared with glutamate group, the expression of Bax protein in hNSC-MVs + glutamate group was significantly down-regulated, and the expression of Bcl-2 protein was remarkably up-regulated(all P<0.01). Conclusion: hNSC-MVs may play a protective role by inhibiting glutamate-induced PC12 cell apoptosis.