摘要
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。
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.
出处
《中国药物与临床》
CAS
2014年第10期1349-1351,共3页
Chinese Remedies & Clinics
