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为探讨六价铬对L-02肝细胞中Caspase-3与Bcl-2表达的影响,将L-02肝细胞暴露于5、10、20μmol/L重铬酸钾溶液,在Caspase-3特异性抑制剂氟甲基酮(Z-DEVD-FMK)与Bcl-2特异性抑制剂ABT-737存在的条件下分别检测Caspase-3以及Bcl-2 mRNA的表达水平以及Caspase-3的活力。结果显示C(rⅥ)处理激活Caspase-3但抑制Bcl-2;Caspase-3抑制剂缓解了Bcl-2表达的下降,Bcl-2抑制剂使原本已被激活的Caspase-3表达进一步升高。提示本实验剂量的C(rⅥ)可诱导L-02肝细胞发生细胞凋亡,且Bcl-2与Caspase-3之间存在负反馈调节作用。
To investigate the effect of hexavalent chromium on the expression of Caspase-3 and Bcl-2 in L-02 hepatocytes, L-02 hepatocytes were exposed to 5, 10 and 20 μmol / L potassium dichromate solution, The expression of Caspase-3 and Bcl-2 mRNA and the activity of Caspase-3 were detected in the presence of Z-DEVD-FMK and Bcl-2 specific inhibitor ABT-737. The results showed that C (rVI) treatment activated Caspase-3 but inhibited Bcl-2; Caspase-3 inhibitor relieved the decrease of Bcl-2 expression; Bcl-2 inhibitor further increased the expression of Caspase-3. These results suggest that C (rVI) can induce apoptosis in L-02 hepatocytes and there is a negative feedback regulation between Bcl-2 and Caspase-3.