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Wistar胎鼠皮层神经元模型及培养神经元缺氧模型 ,用 3种不同浓度的PKC催化亚基特异性抑制剂CalphostinC预孵育培养神经元后进行缺血处理 ,观察神经元下述指标的改变 :神经元存活率、caspase 3(CPP32 )和细胞凋亡的规律。结果 随着缺氧时间的延长和CalphostinC浓度的增加 ,培养神经元的存活数显著下降、caspase 3和TUNEL荧光染色阳性率及平均荧光强度均显著升高。结论 ①PKC和caspase 3均参与了缺氧神经元凋亡 ;②PKC抑制剂CalphostinC可加重缺氧神经元凋亡 ;且该作用是通过caspase 3信号转导途径实现的 ;
Objective To explore the relationship between protein kinase C (PKC) and apoptosis of rat cultured rat neuron due to hypoxia. Methods Neurocortical neuron of fetal rat were cultivated under ischemic and hypoxic condition and 4 different concentrations of Calphostin C, an inhibitor against the catalytic subunit of PKC, were added into the culture media and cultured further for 2 h. The survival rate of neurons, the expression of caspase 3 and the process of apoptosis indicated by TUNEL reaction were observed. Results With the prolonging of hypoxic time and the increasing concentration of Calphostin C, the survival rate of neuron was decreased significantly, and the positive rate of fluorescence staining and the average fluorescent intensity of caspase 3 and TUNEL were significantly increased. Conclusion ①PKC and caspase 3 take part in the process of neuron apoptosis after hypoxia. ② Calphostin C can enhance the hypoxic neuron apoptosis through the signal transduction of caspase 3. ③ The activating of PKC can protect neuron against hypoxic condition.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2001年第1期33-35,共3页
Journal of Third Military Medical University
基金
国家自然科学基金资助项目! (3 9670 2 69)
