自噬参与氧糖剥夺对N2a细胞的损伤

自噬在脑缺血中的作用目前没有统一定论。本文主要是通过建立氧糖剥夺(OGD)模型来模拟脑缺血的过程从而探讨自噬在脑缺血中的作用。在小鼠神经母细胞瘤细胞(N2a)经过OGD处理后,检测处理前后自噬相关蛋白、细胞活力以及乳酸脱氢酶释放率的改变。结果发现在OGD处理后,N2a细胞中微管相关蛋白1轻链3(LC3)、Beclin 1及溶酶体相关膜蛋白2(LAMP2)蛋白表达量均增高,而细胞活力明显下降；与OGD组相比,使用3-甲基腺嘌呤(3-MA)抑制自噬后,N2a细胞乳酸脱氢酶释放率下降。本研究表明在脑缺血过程中自噬被激活,但自噬的激活可能对神经细胞是起损伤性作用的。

Autophagy is involved in the damage of N2a cells by oxygen-glucose deprivation

There is no consensus on the role of autophagy in cerebral ischemia. This article was prompted to explore the effect of autophagy in the process of cerebral ischemia by using the oxygen-glucose deprivation model(OGD) on mouse neuroblastoma cells(N2a)to simulate the cerebral ischemia. Autophagy related proteins expressions, cell viability and cytotoxicity were determined after OGD treatment. Compared with the no-treatment control group, microtubule-associated protein 1 light chain 3(LC3), Beclin 1 and lysosome-associated membrane protein-2(LAMP2) expression were upregulated in OGD group. Cell viability was significantly decreased in OGD group. 3-methyladenine(3-MA) reduced the lactate dehydrogenase release, compared with OGD group. Taken together, the present results indicate that autophagy is activated during cerebral ischemia, and the activation of autophagy may have a damaging effect on the nerve cells.