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目的探讨三氧化二砷(As2O3)联合人参皂甙Rg3对移植瘤肝癌细胞凋亡的影响。方法体外培养人肝癌Bel-7402细胞株,种植于雄性裸鼠皮下,32只鼠随机均分成4组:Rg3组(5、10、20mg/kg)、三氧化二砷组、人参皂甙Rg3+三氧化二砷组(联合用药组)及对照组。实验自肿瘤接种第3天开始,人参皂甙Rg3,隔日灌胃,共20次,三氧化二砷,每次给药为40μg/(kg.d),每日腹腔内注射,连续28d。对照剂为生理盐水。停药一周后,脱颈处死,完整取出瘤块,检测肿瘤的重量,计算抑瘤率。采用免疫组织化学法检测联合用药组、Rg3组、三氧化二砷组及对照组中在裸鼠肝癌移植瘤组织中Bax、Bcl-2蛋白的表达情况。结果三氧化二砷组上调Bax,下调Bcl-2蛋白的表达,作用高于Rg3组,联合组Bcl-2值最低,Bax值最高,随着Rg3药物浓度的升高,联合组的效果更为明显(P<0.05)。结论在裸鼠体内实验中,人参皂甙Rg3与三氧化二砷联合应用,可以显著的抑制人肝癌裸鼠移植瘤的生长,其具体机理可能与下调抑凋亡基因Bcl-2的表达,增强促凋亡基因Bax的表达有关。
Objective To investigate the effects of arsenic trioxide (As2O3) combined with ginsenoside Rg3 on the apoptosis of hepatocellular carcinoma cells. Methods Human hepatocellular carcinoma Bel-7402 cells were cultured in vitro and subcutaneously in male nude mice. Thirty-two mice were randomly divided into 4 groups: Rg3 group (5, 10, and 20 mg / kg), arsenic trioxide group, ginsenoside Rg3 + arsenic trioxide group Group) and control group. Experiments began on the third day after tumor inoculation. Ginsenoside Rg3 was administered intragastrically every other day for 20 times. Arsenic trioxide was administered 40 μg / (kg.d) once daily for 28 days. The contrast agent is saline. One week after discontinuation, the neck was sacrificed, the complete removal of tumor mass, detection of tumor weight, calculation of tumor inhibition rate. Immunohistochemistry was used to detect the expression of Bax and Bcl-2 protein in the transplanted hepatocellular carcinoma in nude mice in combination group, Rg3 group, arsenic trioxide group and control group. Results Arsenic trioxide upregulated Bax and down-regulated the expression of Bcl-2, which was higher than that of Rg3 group. Bcl-2 was the lowest and Bax was the highest in the arsenic trioxide group. The effect was more obvious with the increase of Rg3 concentration (P <0.05). Conclusion The combination of ginsenoside Rg3 and arsenic trioxide can significantly inhibit the growth of human hepatocellular carcinoma xenografts in nude mice in vivo. The specific mechanism may be related to the down-regulation of the expression of the anti-apoptotic gene Bcl-2 and the enhancement of the pro-apoptotic gene Bax expression related.