雷公藤醇提物对人L02肝细胞增殖和凋亡的作用

摘要

目的 研究雷公藤醇提物对人L02肝细胞增殖和凋亡的作用.方法 以0、4、8、16 mg/L的雷公藤醇提物(分别为对照组、4 mg/L组、8 mg/L组、16 mg/L组)干预体外培养的人L02肝细胞48 h后,采用四甲基偶氮唑蓝(MTT)法检测各组肝细胞的生长抑制率,采用膜联蛋白V-异硫氰酸荧光素/碘化吡啶双染流式细胞术检测人L02肝细胞的凋亡率.结果 与对照组比较,4mg/L组的吸光度值降低[(0.90±0.04)比(0.94±0.06),P＜0.05]；当雷公藤醇提物浓度为8 mg/L和16 mg/L时,细胞液吸光度值降低均更加明显[(0.76±0.05)、(0.53 ±0.04)比(0.94±0.06),均P＜0.01].与对照组比较,4 mg/L组的细胞凋亡率升高,差异有统计学意义[(9.68±0.45)％比(5.42±0.27)％,P＜0.05]；当雷公藤醇提物浓度为8mg/L和16 mg/L时,人L02肝细胞凋亡率升高均更加明显[(30.19±0.31)％、(57.26±0.54)％比(5.42±0.27.)％,均P＜0.01].结论 雷公藤醇提物对人L02肝细胞的增殖有抑制作用,并可诱导其凋亡.%Objective To investigate the biological effects of proliferation and apoptosis of human heptical cell line L02 treated by alcohol extract of tripterygium.Methods Proliferative inhibition of L02 incubated with alcohol extract of tripterygium at different concentrations (0,4,8,16 mg/L ) for 48 h was accessed by 3 - (4,5 -Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay.Cell apoptosis was analyzed by Annexin V FITC / PI Flow Cytometry.Results The proliferation of L02 was inhibited by alcohol extract of tripterygium and the inhibition showed a dose-dependent fashion.When the concentration of alcohol extract of tripterygium was 4mg/L,the proliferation of L02 was inhibited at the beginning[(0.90 ±0.04) vs (0.94 ±0.06),P ＜0.05]..When the concentration of alcohol extract of tripterygium reached over 8mg/L,the proliferation of L02 was significantly inhibited [(0.76 ±0.05 ),(0.53 ± 0.04) vs (0.94 ± 0.06 ),all P ＜ 0.01].The percentage of the apoptotic L02 increased after the treatment with alcohol extract of tripterygium and showed dose-dependent fashions as well.When the concentration of alcohol extract of tripterygium was 4mg/L,the percentage of the apoptotic L02 increased at the beginning[(9.68 ±0.45 ) ％ vs (5.42 ± 0.27 ) ％,P ＜ 0.05].When the concentration of alcohol extract of tripterygium reached over 8mg/L,the percentage of the apoptotic L02 increased significantly [( 30.19 ± 0.31 ) ％,( 57.26 ± 0.54 ) ％ vs (5.42 ± 0.27 )％,all P ＜ 0.01].Conclusions Alcohol extract of tripterygium can inhibit proliferation and induce apoptosis in L02 cells.