论文部分内容阅读
目的 研究一氧化氮在鱼藤酮诱导的PC12细胞凋亡中的作用。方法 采用MTT法测定细胞增殖活力及鱼藤酮对PC12细胞的急性损伤效应 ,Greiss法测定NO2 - 含量 ,琼脂糖凝胶电泳检测细胞凋亡。结果 MTT实验表明PC12细胞传代后 7d达到增殖高峰 ,低剂量L NAME对PC12细胞有保护作用 ,在四个不同剂量L NAME的比较试验中 ,10 0μmol L的L NAME对PC12细胞的保护作用最强。鱼藤酮亦可诱导PC12细胞DNA梯带的形成。另外 ,一氧化氮合酶抑制剂L NAME可以抑制鱼藤酮诱导的caspase 3蛋白酶的活力 ,L NAME亦可抑制鱼藤酮诱导的NO的产生。结论 一氧化氮和caspase 3共同参与了鱼藤酮诱导的PC12细胞凋亡
Objective To investigate the role of nitric oxide in rotenone-induced PC12 cell apoptosis. Methods The cell viability and rotenone - induced acute injury of PC12 cells were determined by MTT assay. The NO2 - content was determined by Greiss method and the apoptosis was detected by agarose gel electrophoresis. Results MTT assay showed that the proliferation of PC12 cells reached the peak of proliferation on the 7th day after passage and the low dose of L NAME had protective effect on PC12 cells. L NAME at the concentration of 100μmol L showed the strongest protective effect on PC12 cells in four different doses of L NAME . Rotenone can also induce the formation of DNA ladder in PC12 cells. In addition, nitric oxide synthase inhibitor L NAME can inhibit the activity of rotenone-induced caspase 3 protease, and L NAME can also inhibit rotenone-induced NO production. Conclusion Nitric oxide and caspase 3 participate in rotenone-induced apoptosis of PC12 cells