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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 and mechanism of osthole on human hepatoma cells in vitro. Methods Hep G2 and Huh7 were treated with Osthol. The inhibitory rates of Osthole on these two hepatocellular carcinoma cell lines were determined by MTT assay. The apoptosis of Hep G2 cells was determined by flow cytometry Western blot was used to detect the expression of Cleaved caspase-3, Bcl-2 and Bax in Hep G2 cells. Results The results of MTT assay showed that different concentrations of osthole could inhibit the viability of Hep G2 cells. The results of flow cytometry showed that both high and low doses of osthole could induce apoptosis of Hep G2 cells, Compared with the control group, the low dose osthole group had significant difference (P <0.05). Compared with the same dose of osthole group, z VAD-fmk could effectively inhibit the apoptosis of Hep G2 cells induced by osthole (P <0.05). Osthole could decrease the expression of Bcl-2 in Hep G2 cells significantly (P <0.05), but had no effect on Bax expression. Conclusion Osthole can induce Cleaved caspase-3-dependent apoptosis in hepatocellular carcinoma cells. Osthole could decrease the expression of Bcl-2 and decrease the ratio of Bcl-2 / Bax.