人参皂苷CK诱导人肝癌HepG-2细胞凋亡的研究

Effect of ginsenoside CK on apoptosis of human hepatocellular carcinoma Hep G- 2 cells

目的探讨人参皂苷CK对人肝癌HepG-2细胞凋亡的作用及机制。方法采用MTT法测定不同浓度(30,60,90μmol/L)人参皂苷CK对人肝癌HepG-2细胞的增殖抑制作用;通过HE染色、AO/EB染色观察人参皂苷CK诱导人肝癌HepG-2细胞凋亡的形态学变化;WesternBlotting检测凋亡相关蛋白P53、Bax和Bcl-2的表达情况。结果人参皂苷CK可明显抑制人肝癌HepG-2细胞的增殖,且呈剂量依赖性和时间依赖性。随着人参皂苷CK给药浓度的增加,出现典型凋亡形态特征的细胞逐渐增多,抗凋亡蛋白Bcl-2和P53表达量逐渐下降,而促凋亡蛋白Bax的表达逐渐升高,Bcl-2/Bax比例明显降低。结论人参皂苷CK可诱导人肝癌HepG-2细胞凋亡,其作用机制可能与下调P53蛋白表达和降低Bcl-2/Bax比例有关。

Objective To investigate the effect of ginsenoside CK on apoptosis of human hepatocellular carcinoma Hep G- 2 cells and the mechanism. Methods human hepatocellular carcinoma Hep G- 2 cells were treated with different doses（ 30,60,90μmol /L） of ginsenoside CK. Cell growth inhibitive rate was measured by MTT assay; Morphological changes of Hep G- 2 cells were observed by HE staining and AO / EB staining; The protein expression of P53,Bax and Bcl- 2 were analyzed by western blotting. Results Ginsenoside CK inhibited proliferation of Hep G- 2 cells in dosage- dependent manner and time- dependent manner. In comparison with control group,treated groups altered cell morphology and detected apoptosis of tumor cells,and the expression of P53 and Bcl- 2 were decreased obviously and Bax was elevated by western blotting. Conclusion Ginsenoside CK induce apoptosis of human hepatocellular carcinoma Hep G- 2 cells and the main mechanism are related to cut P53 protein and reduce Bcl- 2 / Bax ratio.