高车前素对肝癌细胞增殖的抑制作用及作用机制研究

目的研究高车前素对肝癌细胞增殖的抑制作用,检测高车前素对Janus蛋白酪氨酸激酶/信号转导和转录活化蛋白(JAK/STAT3)信号通路的影响。方法采用四甲基偶氮唑盐(MTT)法检测不同浓度高车前素(1,5,10,25,50,100,200μmol/L)对Bel-7402肝癌细胞株增殖的影响。高车前素(5,25,100μmol/L)预处理Bel-7402肝癌细胞48 h,采用Transwell小室检测各组细胞的体外侵袭能力,蛋白印迹法检测p-STAT3、Twist1和Bcl-2蛋白表达差异。结果高车前素能浓度依赖性抑制Bel-7402肝癌细胞株增殖。高车前素(25,100μmol/L)预处理能显著减弱Bel-7402肝癌细胞的体外侵袭力,抑制p-STAT3、Twist1和Bcl-2蛋白表达(P<0.05)。结论高车前素可能通过JAK/STAT3通路,抑制p-STAT3、Twist1蛋白活性表达,从而抑制抗凋亡的Bcl-2蛋白表达,来发挥有效抑制肝癌细胞增殖的作用。

Inhibitory efficiency and mechanisms of hispidulin on proliferation of hepatoma cells

Objective To determine the inhibitory efficiency of hispidulin on proliferation of hepatoma cells, and to assess the influence of hispidulin on JAK /STAT3 signaling. Methods The MTT assay was applied to detect the effects of different concentrations （1, 5, 10, 25, 50, 100 and 200 μmol/L） of hispidulin on Bel-7402 hepatoma cell line proliferation. The Bel-7402 hepatoma cells were pretreated by hispidulin （5, 25,100 μmol/L） for 48 h, followed by the in vitro invasiveness test by using the Transwell chamber. Western blotting was employed to detected the expres-sion of p-STAT3, Twist1 and Bcl-2 protein expression. Results Hispidulin inhibited the proliferation of Bel-7402 hepatoma cells in a concentration-dependent fashion. Pretreatment by hispidulin （25,100 μmol/L） resulted in signifi-cantly reduced in vitro invasiveness of Bel-7402 hepatoma cells, and markedly attenuated expression of p-STAT3, Twist1 and Bcl-2 protein （all P〈0.05）. Conclusion Hispidulin effectively attenuates the expression of p-STAT3, Twist1 protein, and inhibits the expression of anti-apoptotic Bcl-2 protein by JAK /STAT3 signaling, thus inhibiting the proliferation of liver cancer cells.