水飞蓟宾诱导人肝癌细胞HepG2死亡及机制研究

Silibinin Induced Cell Death in Hepatoma Cell line HepG2 and Its Mechanism

目的探讨水飞蓟宾对人肝癌细胞HepG2的杀伤作用及其机制。方法不同浓度水飞蓟宾处理HepG2细胞,采用MTT法检测HepG2细胞增殖情况,流式细胞术检测水飞蓟宾诱导HepG2细胞的凋亡情况。利用ROS荧光探针二氢乙啶(DHE)检测水飞蓟宾是否诱导HepG2细胞ROS的产生,并用ROS抑制剂抗坏血酸预处理后检测水飞蓟宾对HepG2的杀伤活性及诱导凋亡的能力。结果水飞蓟宾可显著抑制HepG2细胞的增殖并诱导其发生凋亡。水飞蓟宾处理后HepG2细胞的ROS显著增高(P<0.05,P<0.01),用抗坏血酸预处理后水飞蓟宾对HepG2的增殖抑制作用降低,并抑制水飞蓟宾诱导的凋亡。结论水飞蓟宾通过诱导ROS的产生引起人肝癌细胞发生凋亡。

Objective To investigate the effect of silibini on proliferation of HepG2 cells and the underlying mechanism. Methods HepG2 cells were treated with various concentrations of silibinin; then the proliferation of HepG2 cells treated with silibinin was determined by using MMT assay and the apoptosis of HepG2 cells was de-tected by flow cytometry. The generation of ROS in HepG2 cells induced by silibinin was observed by using fluo-rescent probe with DHE and then was inhibited by ascorbic acid to observe whether the effect of silibinin on pro-liferation of HepG2 cells was dependent on ROS. Results Silibinin significantly inhibited the proliferation of HepG2 cells, inducing apoptotic cell death. The ROS significantly increased in HepG2 cells treated with silibinin （P〈0.05, P〈0.01）. After ascorbic acid treatment, the suppression as well as apoptosis of HepG2 cells induced by silibinin decreased. Conclusion Silibinin can induce apoptotic cell death of HepG2 cells via upregulating ROS.