摘要
目的探讨蛇床子素体外对人肝癌细胞的杀伤效应及机制。方法将人肝癌细胞系Hep G2和Huh7用蛇床子素治疗后,采用MTT法检测蛇床子素对这2种肝癌细胞系的抑制率,采用流式细胞术检测蛇床子素对Hep G2细胞凋亡的影响,采用Western blot法检测蛇床子素对Hep G2细胞Cleaved caspase-3、Bcl-2和Bax的表达。结果 MTT试验结果表明,不同浓度的蛇床子素均能抑制Hep G2细胞的细胞活力;流式细胞实验结果表明,高、低剂量的蛇床子素均能诱导Hep G2细胞发生凋亡,且高、低剂量蛇床子素组与对照组相比差异均有统计学意义(P<0.05);与相同剂量蛇床子素组比较,z VAD-fmk可有效抑制蛇床子素对Hep G2细胞的凋亡诱导效应,差异有统计学意义(P<0.05);蛇床子素能显著降低Hep G2细胞Bcl-2的表达水平,差异有统计学意义(P<0.05),但对Bax表达无影响。结论蛇床子素诱导肝癌细胞进入Cleaved caspase-3依赖的凋亡过程,其机制可能为蛇床子素可显著降低Bcl-2表达,从而降低Bcl-2/Bax比例。
Objective To investigate the killing effect of osthole in vitro on human hepatocellular carcinoma cells and its mechanism. Methods Hep G2 and Huh7 cells were treated with osthole. Cell viability was then measured using the MTT assay. Apoptosis of Hep G2 treated with osthole was determined by flow cytometry. The expression of Cleaved caspase- 3,Bcl- 2 and Bax was detected by Western blot. Results The results of MTT assay indicated that the viability of Hep G2 cells could be inhibited by different concentrations of osthole. The results of apoptosis detected by flow cytometry showed that both the high concentration and the low concentration of osthole could induce apoptosis in Hep G2 cells,compared with the control group（ P〈0. 05）. Compared with the equal dose of osthole group,z VAD- fmk significantly inhibited the apoptosis induced by osthole,and the difference had statistical significance（ P〈0. 05）. Osthole could significantly reduce the Hep G2 cells of Bcl- 2 expression level,the difference was statistically significant（ P〈0. 05）,but there was no effect on the expression of Bax. Conclusion Osthole induced Cleaved caspase- 3 dependant apoptosis whose mechanism could significantly reduce the expression of Bcl- 2,thereby reducing the proportion of Bcl- 2 / Bax.
出处
《中国卫生检验杂志》
CAS
2015年第19期3259-3261,共3页
Chinese Journal of Health Laboratory Technology
