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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 the apoptosis of HepG-2 cells and its mechanism. Methods MTT assay was used to determine the effects of different concentrations of ginsenoside CK on the proliferation of HepG-2 cells. HE staining and AO / EB staining were used to observe the effects of ginsenoside CK on HepG-2 cells The morphological changes of apoptotic cells were detected by Western Blotting. The expressions of apoptosis-related proteins P53, Bax and Bcl-2 were detected by Western Blotting. Results Ginsenoside CK could significantly inhibit the proliferation of HepG-2 cells in a dose-and time-dependent manner. With the increase of ginsenoside CK concentration, the cells with typical morphological features of apoptosis gradually increased, the expression of anti-apoptotic proteins Bcl-2 and P53 gradually decreased, while the expression of pro-apoptotic protein Bax gradually increased. The expression of Bcl- 2 / Bax ratio decreased significantly. Conclusion Ginsenoside CK can induce apoptosis in HepG-2 human hepatocellular carcinoma cells. Its mechanism may be related to down-regulation of P53 protein expression and decrease of Bcl-2 / Bax ratio.