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目的研究吉马酮抑制肝癌Bel7402细胞增殖的作用机理。方法通过MTT法比较吉马酮对Bel7402和L02细胞增殖的影响,流式细胞仪检测并确定吉马酮对Bel7402细胞凋亡和活性氧含量的影响。Western-blot法检测吉马酮处理前后p53、Bax和Bcl-2蛋白合成的变化。结果实验浓度范围内,吉马酮可选择性浓度依赖性的抑制Bel7402细胞的增殖;吉马酮剂量依赖性的促进肝癌Bel7402细胞凋亡和上调活性氧含量;吉马酮显著促进抑癌蛋白p53和Bax的表达,抑制抗凋亡蛋白Bcl-2的表达。结论吉马酮在体外能明显抑制肝癌Bel7402细胞的增殖,上述变化可能通过上调p53和Bax、下调Bcl-2及上调活性氧含量来完成。
Objective To study the mechanism of the inhibitory effect of germacrone on the proliferation of Bel7402 hepatocellular carcinoma cells. Methods MTT assay was used to compare the effects of germacrone on the proliferation of Bel7402 and L02 cells. Flow cytometry was used to determine the effect of germacrone on apoptosis and reactive oxygen species in Bel7402 cells. Western-blot was used to detect the changes of p53, Bax and Bcl-2 protein synthesis before and after germatrine treatment. Results In the experimental concentration range, germacrone inhibited the proliferation of Bel7402 cells selectively and in a concentration-dependent manner. Gemcitabine promoted the apoptosis of Bel7402 cells and up-regulated the content of reactive oxygen species in a dose-dependent manner. And Bax expression, inhibit the expression of anti-apoptotic protein Bcl-2. Conclusions Gemcitabine can significantly inhibit the proliferation of Bel7402 cells in vitro. The above changes may be caused by the up-regulation of p53 and Bax, down-regulation of Bcl-2 and up-regulation of reactive oxygen species.