论文部分内容阅读
目的 探讨蛋白激酶C(PKC)对神经元缺氧凋亡的影响及作用机制。方法 建立体外培养大鼠皮层神经元模型及培养神经元缺氧模型 ,用三种不同浓度的PKC催化亚基特异性抑制剂ClphostinC预孵育培养神经元后进行缺血处理 ,观察神经元胞膜PKC(mPKC)活性、Bcl 2表达和TUNEL表达 (细胞凋亡 )的规律。结果 随着缺氧时间的延长mPKC活性显著增加 ,同时伴随缺氧时间的延长和ClphostinC浓度的增加 ,培养神经元Bcl 2的表达显著下降、TUNEL荧光染色阳性率显著升高。结论 ①mPKC的活化和Bcl 2表达均参与了缺氧神经元凋亡 ;②缺氧和PKC抑制剂ClphostinC可加重缺氧神经元凋亡 ;且该作用是通过抑制抗凋亡蛋白Bcl 2表达实现的 ;③PKC的激活在缺氧神经元凋亡中起保护作用
Objective To investigate the effect and mechanism of protein kinase C (PKC) on neuronal apoptosis induced by hypoxia. Methods The rat cortical neuron model was cultured in vitro and the neuronal hypoxia model was established. The neurons were preincubated with three different concentrations of PKC catalytic subunit specific inhibitor ClphostinC for ischemic treatment. The expression of PKC (mPKC) activity, Bcl 2 expression and TUNEL expression (apoptosis). Results The mPKC activity was significantly increased with hypoxia time. With the prolongation of hypoxia time and the increase of Clphostin C concentration, the expression of Bcl - 2 in neurons decreased significantly, and the positive rate of TUNEL fluorescence staining increased significantly. Conclusion ① The activation of mPKC and the expression of Bcl 2 are involved in the apoptosis of hypoxic neurons; ② Hypoxia and PKC inhibitor ClphostinC can increase the apoptosis of hypoxic neurons; and this effect is achieved by inhibiting the expression of anti-apoptotic protein Bcl 2 ; ③ PKC activation plays a protective role in hypoxic neuronal apoptosis