蛇床子素通过上调抑癌基因PTEN抑制肝癌细胞HepG2增殖并促进细胞凋亡

目的:探究蛇床子素对肝癌细胞Hep G2增殖及凋亡的作用及作用机制。方法:用不同浓度蛇床子素处理肝癌细胞,CCK8检测细胞活性,流式检测细胞凋亡,Western blot检测细胞增殖、凋亡标记蛋白及PTEN的表达;同时用PTEN抑制剂bp V(HOpic)处理细胞,CCK8和流式再次检测细胞增殖及凋亡情况。结果:100μmol/L蛇床子素作用4 d和5 d能明显降低细胞增殖倍数(P<0. 05),150μmol/L蛇床子素作用3 d、4 d和5 d也可显著降低细胞增殖倍数(P<0. 05,P<0. 01),并且蛇床子素(100μmol/L,150μmol/L)还能显著抑制细胞增殖标记蛋白Ki67和PCNA的表达,并体现量效关系(P<0. 05,P<0. 01);同时,蛇床子素(100μmol/L,150μmol/L)能明显促进肝癌细胞凋亡及凋亡标记蛋白Bax表达,降低Bcl-2蛋白表达水平(P<0. 05,P<0. 01);此外,蛇床子素(100μmol/L,150μmol/L)还能显著促进抑癌基因PTEN的表达(P<0. 05,P<0. 01);bp V(HOpic)能明显减弱蛇床子素对肝癌细胞增殖的抑制作用及对细胞凋亡的促进作用(P<0. 05)。结论:蛇床子素能通过上调PTEN表达抑制肝癌细胞Hep G2增殖、促进肝癌细胞凋亡。

Osthole inhibits proliferation and induces apoptosis of hepatocellular carcinoma cell line HepG2 via upregulating PTEN

Objective:To investigate the effects and mechanism of osthole on proliferation and apoptosis in a hepatocellular carcinoma cell(HCC)line HepG2.Methods:Treated cells with osthole at different concentrations.Cell viability was measured by CCK8 assay and apoptosis was detected by flow cytometry.Western blot was performed for calculating the expression levels of proliferation-related,apoptosis-related proteins and PTEN.After pretreatment with bpV(HOpic),cell proliferation and apoptosis were measured again.Results:Treatment with osthole(100μmol/L)for 4 and 5 days inhibited cell viability of HCC markedly(P<0.05,P<0.01).Osthole(150μmol/L)decreased cell viability of HCC with a time-dependently manner and also decreased the expressions of Ki67 and PCNA(P<0.05,P<0.01).Meanwhile,treatment with osthole(100μmol/L,150μmol/L)induced apoptosis of HCC significantly coupled with increasing Bax and decreasing Bcl-2(P<0.05,P<0.01).In addition,osthole(100μmol/L,150μmol/L)up-regulated the protein level of PTEN(P<0.05,P<0.01).Furthermore,pretreatment with bpV(HOpic)(1μmol/L)notably reversed the inhibitory effect on proliferation and promotive effect on apoptosis of osthole(P<0.05).Conclusion:Osthole inhibits cell proliferation and induces apoptosis of HCC by up-regulating the protein level of PTEN.