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目的 探讨NDGA诱导胃癌细胞凋亡的分子机制。方法 分光光度法检测caspase 3的细胞活性 ,同时用Westernblot分析caspase 3及其底物PARP。用Westernblot分析P5 3、caspase 3、PARP、P2 1wafl、P2 7kipl、Bcl 2和Bax的浓度。免疫法检测细胞色素C。结果 NDGA通过活化caspase 3诱导细胞凋亡 ,caspase 3的活化是由于细胞色素C从线粒体释放入细胞质而引起的。NDGA处理也可导致P2 7kipl、Bax蛋白水平升高 ,同时伴有细胞积聚于G1期。z DEVD fmk ,一种caspase 3抑制剂 ,可逆转caspase 3的活化及其引起的凋亡。结论 NDGA诱导的细胞凋亡是通过上调P2 7kipl、Bax的水平 ,释放细胞色素C ,最终活化caspase 3而引起的
Objective To explore the molecular mechanism of NDGA-induced gastric cancer cell apoptosis. Methods The cellular activity of caspase 3 was measured by spectrophotometry. At the same time, caspase 3 and its substrate PARP were analyzed by Western blot. Western blot was used to analyze the concentrations of P5 3, caspase 3, PARP, P2 1wafl, P2 7kipl, Bcl 2 and Bax. Immunodetection of cytochrome C. Results NDGA induced apoptosis through activation of caspase 3. The activation of caspase 3 was caused by the release of cytochrome C from the mitochondria into the cytoplasm. NDGA treatment can also lead to elevated levels of P2 7kipl and Bax proteins, accompanied by accumulation of cells in the G1 phase. z DEVD fmk, a caspase 3 inhibitor, reverses the activation of caspase 3 and its induction of apoptosis. Conclusion NDGA-induced apoptosis is caused by up-regulation of P2 7kipl and Bax levels, release of cytochrome C, and activation of caspase 3