摘要目的 观察千层纸素A对肝癌细胞MHCC97-H增殖和凋亡的影响,并探讨其分子机制.方法 通过噻唑蓝(MTT)法检测MHCC97-H细胞增殖能力;通过碘化丙锭(PI)/膜联蛋白Ⅴ-异硫氰酸荧光素(Annexin Ⅴ-FITC)双染法检测MHCC97-H细胞凋亡率;通过Western blot检测相关蛋白表达水平.结果 3种浓度千层纸素A均可抑制MHCC97-H细胞的增殖能力,千层纸素A对MHCC97-H细胞增殖的抑制作用具有浓度依赖性;50、100和150 μmol/L千层纸素A处理后MHCC97-H细胞凋亡率分别为(18.87±0.37)％、(20.93±0.32)％、(24.37±0.47)％;100、150 μmol/L千层纸素A处理后MHCC97-H细胞的腺苷酸活化蛋白激酶(AMPK)蛋白表达下降.结论 千层纸素A抑制肝癌细胞的增殖,促进细胞凋亡,并下调AMPK蛋白表达.

abstractsObjective To investigate the effectof oroxylin on cell proliferation and apoptosiof hepatomcellMHCC97-H and demonstrate the moleculamechanism underlying effectof oroxylin A.MethodCell proliferation waexamined by methyl thiazol tetrazolium (MTT) assay.The apoptosirate waevaluated by propidium iodide (PI)/Annexin Ⅴ-fluoresceine isothiocyanate (FITC) double staining method.The protein levelof AMP-activated protein kinase (AMPK) were examined by Western blotting,respectively.Result50, 100 and 150 μmol/L oroxylin inhibited cell proliferation of MHCC97-H cellin concentration-dependenmanner.The apoptosirate of MHCC97-H cellexposed to 50, 100 and 150 μmol/L oroxylin wa(18.87 ± 0.37)％, (20.93 ± 0.32)％ and (24.37 ± 0.47)％, respectively.100 and 150 μmol/L oroxylin caused decreased accumulation and phosphorylation of AMPK in MHCC97-H cells.Conclusion Oroxylin inhibitcell proliferation and induceapoptosiof MHCC97-H cellby regulating AMPK signaling pathway.