中文摘要：

目的：探讨缺氧处理对神经干细胞（NSCs）凋亡的影响及其作用机制。方法：采用无血清培养法培养新生大鼠NSCs，采用流式细胞术检测NSCs的凋亡率和线粒体跨膜电位，采用免疫印记法检测凋亡执行蛋白Caspase-3和线粒体通路相关蛋白Bcl-2，Bax的表达。结果：缺氧组的早期凋亡率高于正常组，线粒体跨膜电位降低，差异有统计学意义（P〈0．05）；缺氧条件下Caspase-3、Bax表达升高，Bcl-2表达降低，差异均有统计学意义（P〈0．05）。结论：缺氧可诱发NSCs凋亡，其作用机制可能是通过上调线粒体通路中促凋亡蛋白Bax的表达，下调Bcl-2的表达，最终激活凋亡蛋白Caspase-3，为缺血缺氧性脑损伤病理机制的阐明奠定基础。

英文摘要：

Objective： To study the underlying mechanism of apoptosis of NSCs under hypoxia in vitro. Methods： The NSCs isolated from infant rat brain were cultured by serum-free medium in vitro. The apoptotic rate and the mitochondrial trans-membrane potential of NSCs were detected by FCM. The expression of apoptotic executive protein Caspase-3, Bcl-2 and Bax related to the mitochondrial path- way were detected by Western blot. Results： Compared with normal control group, the apoptotic rate and the mitochondrial trans-mem- brane potential of NSCs decreased significantly （P〈0.05）. The expression of Caspase-3 and Bax increased after hypoxia, while the ex- pression of Bcl-2 decreased （P〈0.05）. Conclusion： Hypoxia can induce NSC apoptosis via activating apoptotic executive protein Cas- pase-3 which is regulated by Bcl-2 and Bax. This study will help to elucidate molecular raechanisms of hypoxic-ischemic brain injury.