中文摘要：

目的 研究人参皂苷Rk3对肝癌HepG2细胞凋亡影响。方法 体内实验采用HepG2细胞裸鼠腋部皮下接种,制备荷瘤鼠肝癌模型,分为生理盐水组、人参皂苷Rk3（25、50、100mg/kg）组和5-氟尿嘧啶（5-Fu,20mg/kg）组;体外实验分为正常组、人参皂苷Rk3（20、40、80μmol/L）组和5-Fu（50μg/ml）组;MTT法检测HepG2细胞增殖;流式细胞术检测HepG2细胞凋亡;RT-PCR法检测HepG2细胞中Bax、Bcl-2,cleaved-Caspase-3、DR4和DR5mRNA表达;Westernblot法检测HepG2细胞中Bax、Bcl-2、cleaved-Caspase-3、DR4和DR5蛋白表达。结果 人参皂苷Rk3（100mg/kg）够明显抑制瘤体重量（P〈0.05）;人参皂苷Rk3（20、40、80μmol/L）能明显抑制HepG2细胞增殖,诱导HepG2细胞凋亡;人参皂苷Rk3（20、40、80μmol/L）能显著增加Bax、cleved-Caspase-3、DR4和DR5蛋白和mRNA的表达,降低Bcl-2蛋白和mR-NA的表达（P〈0.05）。结论 人参皂苷Rk3可能通过DR4、DR5诱导HepG2细胞凋亡。

英文摘要：

Objective To study the effect of ginsenoside Rk3 on apoptosis of HepG2. Methods Tumor bearing mice model of liver cancer was prepared inoculating HepG2 cells in axilla of nude mice subcutaneously. The nude mice were grouped into saline group, ginsenoside Rk3 （25, 50 ,100 mg/kg） group and 5-Fu （20 mg/kg） group in vivo. And the HepG2 cells were divided into normal group, ginsenoside Rk3 （20, 40, 80 μmol/L） group and 5- Fu（50 μg/ml） group in vitro. The inhibition rate of HepG2 cells was evaluated by MTT assay. The apoptosis distribution of HepG2 cells was detected by flow cytomtric analysis. The mRNA expressions of Bax, Bcl-2, cleaved- Caspase-3, DR4 and DR5 in HepG2 cells were detected by RT-PCR. The protein expressions of Bax, Bcl-2 cleaved-Caspase-3, DR4 and protein in HepG2 cells were observed by Western blot. Results Ginsenoside Rk3 （100 mg/kg） significantly inhibited tumor weight（P 〈 0. 05 ）. Ginsenoside Rk3 （20, 40 and 80 ~mol/L） significantly inhibited the proliferation and induced apoptosis in HepG2 cells. Ginsenoside Rk3 （20, 40 and 80 ~mol/L） significantly increased Bax, cleaved-Caspase-3 DR4 expression and DR5 mRNA and protein, reduced the expression of Bcl-2 mRNA and protein. The difference was statistically significant. Conclusion Ginsenoside Rk3 can induce apoptosis of HepG2 cells possibly through the DR4 and DR5.