摘要
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 ;
Objective To explore the effect and possible mechanism of protein kinase C (PKC) on the apoptosis of cultured neurons after hypoxia Methods Model of cultured rat neurons under hypoxia condition was established. Calphostin C, an inhibitor for the catalytic subunit of PKC, at 4 different concentrations were separately cocultured for 2 h with the neurons having been cultivated under hypoxic condition for different times The activity of membrane PKC (mPKC), the expression of Bcl 2 and the situation of neuron apoptosis were studied Results With the prolonging of hypoxic time the activity of mPKC was increased significantly And the expression of Bcl 2 was decreased obviously and positive rate of TUNEL were significantly increased in a calphostin C concentration dependent manner Conclusion ① The activation of mPKC and Bcl 2 are involved in the apoptosis of neurons after hypoxia ② Hypoxia and calphostin C can aggravate the hypoxic neuronal apoptosis through the signal transduction of Bcl 2 ③ The activation of PKC can protect neuron against hypoxia
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2002年第12期1399-1401,共3页
Journal of Third Military Medical University
基金
国家自然科学基金资助项目 ( 396 70 2 6 9)
