Bcl-2和Bax在多巴胺诱导PC12细胞凋亡中的作用

目的探讨多巴胺诱导PC12细胞凋亡的可能机制。方法流式细胞仪检测PC12细胞的凋亡率及Bcl-2和Bax蛋白的表达率。结果多巴胺诱导PC12细胞凋亡，两者间呈明显的量效和时效关系。0.45mmol/L多巴胺作用24h，细胞的凋亡率为53.3%±3.1%。在凋亡过程中，Bcl-2蛋白表达显著降低，Bax蛋白表达随之增高。诱导型一氧化氮合成酶(iNOS)抑制剂和半胱氨酸蛋白酶3(CPP32)抑制剂对抗多巴胺诱导PC12细胞的凋亡作用与Bcl-2蛋白增加、Bax蛋白降低有关。结论Bcl-2和Bax蛋白是多巴胺诱导PC12细胞凋亡的重要调节蛋白，iNOS和CPP32在凋亡过程中可能具有重要作用。

The effect of Bcl-2 and Bax proteins on dopamine-induced apoptosis in PC12 cells

Objective　To explore the possible mechanism of dopamine-induced apoptosis in PC12 cells. 　Methods　 Flow cytometric assay was used to quantitate the apoptotic cells and measure the positive rates of Bcl-2 and Bax proteins in PC12 cells. 　Results　 Dopamine induced PC12 cell apoptosis in a dosage- and time-dependent manner. After 24 h treatment with 0.45 mmol/L dopamine, the percentage of apoptotic PC12 cells was 53.30%±3.14%. During the apoptotic process, it showed a decrease of Bcl-2 protein and an increase of Bax protein in PC12 cell. Inhibitors of iNOS (inducible nitric oxide synthase, iNOS) and Caspase-3 (cysteinyl aspantate-specific proteinases-3, Caspase-3 or CPP32) blocked PC12 cells apoptosis by increasing expression of Bcl-2 and decreasing expression of Bax. 　Conclusions　 Bcl-2 and Bax proteins might be important regulators in dopamine-induced apoptosis in PC12 cells. iNOS and CPP32 might play an important role in the apoptotic process.