白凤菜总黄酮对肝癌HepG2细胞生长、增殖和凋亡的影响

(1.漳州卫生职业学院基础医学部,福建 漳州 363000; 2.厦门大学生命科学学院,福建 厦门 361102)

白凤菜; 总黄酮; 细胞增殖; 细胞周期; 细胞凋亡

Influence of total flavonoids of Gynura formosana Kitam.on the growth,proliferation and apoptosis of hepatoma HepG2 cells
LIN Yanyan1,XU Xinheng2,HUANG Zhongqing1,LIN Zeyan1,

(1.Faculty of Basic Medicine,Zhangzhou Health Vocational College,Zhangzhou 363000,China; 2.School of Life Sciences,Xiamen University,Xiamen 361102,China)

Gynura formosana Kitam.; total flavonoids; cell proliferation; cell cycle; cell apoptosis

DOI: 10.6043/j.issn.0438-0479.201807007

备注

研究了白凤菜(Gynura formosana Kitam.)总黄酮(TFG)对肝癌HepG2细胞的生长、增殖和凋亡的影响.噻唑兰(MTT)实验结果表明TFG对HepG2细胞体外增殖的抑制作用有浓度和时间依赖效应:处理24 h后130和260 μg/mL TFG实验组的HepG2细胞凋亡率均显著升高,分别达到(47.00±1.31)%和(76.39±1.39)%(p<0.05); 24 h的半抑制质量浓度(IC50)为190.80 μg/mL.实验组HepG2细胞周期阻滞在S期,细胞迁移率随TFG质量浓度的升高而下降,细胞内活性氧(ROS)水平最终显著下降至对照组的6.9%(p<0.05),细胞中Bax表达量略微上调而Bcl-2表达量明显下调.综上,TFG抑制肝癌HepG2细胞增殖和诱导HepG2细胞凋亡的机制可能与下调细胞ROS水平、重构细胞内还原体系、上调促凋亡蛋白Bax以及下调凋亡抑制蛋白Bcl-2表达相关.

This paper investigated the effects of total flavonoids of Gynura formosana Kitam.(TFG)on the growth,proliferation and apoptosis of hepatoma HepG2 cells.The MTT assay detected that TFG had dose- and time-dependent effects on the proliferation inhibition of HepG2 cells.The apoptosis rates of HepG2 cells treated with TFG of 130 μg/mL and 260 μg/mL increased significantly to(47.00±1.31)% and(76.39±1.39)%,respectively(p<0.05),and the half-concentration of inhibition(IC50)in 24 h was 190.80 μg/mL.In the TFG-treated groups, the HepG2 cell cycle was remarkably retarded and stayed in S phase and the cell mobility decreased with the increasing TFG concentration; the reactive oxygen species(ROS)levels of the HepG2 cells finally declined to 6.9%(p<0.05); the Bax expression in cells was slightly up-regulated and Bcl-2 expression was obviously down-regulated.Taking together,the mechanism inhibiting the proliferation and inducing the apoptosis of HepG2 cells may be related to the reduction in the ROS levels,the rebuilding of the intracellular redox system,the up-regulation of apoptosis promoting protein Bax and down-regulation of apoptosis inhibiting protein Bcl-2.