白毛藤对人肝癌Bel7402细胞增殖抑制及凋亡作用

Effects of Solamum lyratum Thunb on proliferation and apoptosis of human hepatocellular carcinoma Bel7402 cells

目的探讨白毛藤体外对人肝癌Bel7402细胞增殖与凋亡的影响及其作用机制。方法采用四甲基偶氮噻唑蓝(MTT)法和荧光显微镜观察白毛藤对人肝癌Bel7402细胞的增殖抑制作用和其诱导Bel7402细胞凋亡情况;用反转录-聚合酶链式反应(RT-PCR)检测survivin、bax基因表达量的变化。结果随白毛藤浓度增加、作用时间延长,对人肝癌Bel7402细胞的增殖抑制作用均明显增强(P<0.01);4,8,16 mg/mL白毛藤组人肝癌Bel7402细胞凋亡率分别为10.98%、17.02%、26.78%,均高于对照组6.18%(P<0.01);作用48 h后,4,8,16 mg/mL白毛藤组人肝癌Bel7402细胞中survivin基因灰度比值分别为(0.43±0.01)、(0.38±0.02)、(0.29±0.01),均低于对照组(0.65±0.05),差异均有统计学意义(P<0.01);4,8,16 mg/mL白毛藤组人肝癌Bel7402细胞中bax基因灰度比值分别为(0.47±0.05)、(0.56±0.04)、(0.73±0.06),均高于对照组(0.36±0.02),差异均有统计学意义(P<0.01)。结论白毛藤可抑制人肝癌Bel7402细胞增殖、诱导其细胞凋亡,并能调控survivin及bax基因的表达。

Objective To observe the effects and the metabolism of Solamum lyratum Thunb on proliferation and apoptosis of Bel7402 cells in vitro. Methods The inhibitory effects of Solamum lyratum Thunb on proliferation of Bel7402 cells were measured by methy thiazolyl tetrazolium（MTT） colorimetric assay.Bel7402 cells were treated with various doses of Solamum lyratum Thunb.We observed apoptosis of Bel7402 cells with fluorescence microscope and detected the levels of survivin and bax gene expression with reverse transcriptase（RT）-PCR. Results Solamum lyratum Thunb inhibited the proliferation of Bel7402 cells（P0.01）.The apoptosis rates of Bel7402 cells in different dose groups（4,8,16 mg/mL） were 10.98%,17.02%,and 26.78%,respectively,and the rates were significantly higher than that of the control group（6.18%,P0.01）.After 48 hours,the levels of survivin gene expression in different dose groups were 0.43±0.01,0.38±0.02,and 0.29±0.01,respectively,and were significantly lower than that of the control group（0.65±0.05,P0.01）.The levels of bax gene expression in different dose groups were 0.47±0.05,0.56±0.04,and 0.73±0.06,respectively,and were significantly higher than that of the control group（0.36±0.02,P0.01）. Conclusion Solamum lyratum Thunb has anti-tumor effect on Bel7402 cells and could induce apoptosis of Bel7402 cells probably through down-regulatoin of survivin gene expression and up-regulation of bax gene expression.