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目的 探讨人参皂甙 Rg3对大鼠诱发性肝癌的作用及其机制。方法 建立 SD大鼠诱发性肝癌模型 ,经肿瘤供血动脉灌注不同剂量的 2 0 (R) -人参皂甙 Rg3(0 .375、1.5、6 .0 mg/ kg) ,磁共振成像 (MRI)技术测量治疗前、后肿瘤的体积变化 ,流式细胞仪 (FCM)和免疫组织化学方法检测肿瘤细胞的凋亡、增殖及坏死情况。结果 高剂量组对肿瘤体积的影响与对照组比较 ,其差异具有显著性 (P<0 .0 5 ) ;低、中、高三个治疗组诱导大鼠肝癌细胞的平均凋亡率 (% )分别为 11.0 8± 3.78、13.5 7± 3.34和 2 7.35± 16 .0 4 ,高剂量组较其它组差异显著 ;用药后测得 S期细胞的平均比率 (% )分别为 2 3.98± 9.4 4、19.73± 6 .6 2和 14 .0 9± 3.4 8,治疗组与对照组相比均有显著性差异 ,且药物剂量与其对肿瘤细胞的抑制作用呈正相关。高剂量组中增殖细胞核抗原 (PCNA)与肿瘤坏死因子 (TNF)的表达与对照组相比差异有显著性 ;治疗组组间 PCNA与 TNF的表达差异不显著。结论 经肿瘤供血动脉灌注人参皂甙 Rg3能明显的抑制肿瘤细胞增殖、有效的诱导肿瘤细胞凋亡、促进肿瘤组织坏死 ,并有剂量依赖性。
Objective To investigate the effect of ginsenoside Rg3 on induced hepatocellular carcinoma in rats and its mechanism. Methods The model of induced hepatocellular carcinoma in SD rats was established. Twenty different doses of Rg3 (0. 375,1.5,6. 0 mg / kg) were infused through the feeding artery of the tumor, and measured by magnetic resonance imaging (MRI) The changes of tumor volume before and after treatment, the apoptosis, proliferation and necrosis of tumor cells were detected by flow cytometry (FCM) and immunohistochemistry. Results The effect of high dose group on tumor volume was significant compared with that of control group (P <0.05). The average apoptosis rate (%) of hepatoma cells induced by low, middle and high dose of three groups were respectively 11.0 8 ± 3.78,13.5 7 ± 3.34 and 2 7.35 ± 16 .0 4, the high-dose group was significantly different from other groups; the average percentage (%) of S-phase cells measured after treatment was 23.9 ± 9.4 4 and 19.73 ± 6 .62 and 14 .0 9 ± 3.4 8, the treatment group and the control group were significantly different, and the drug dose and its inhibition of tumor cells was positively correlated. The expression of PCNA and TNF in the high dose group had significant difference compared with the control group. There was no significant difference between the two groups in the expression of PCNA and TNF. Conclusion Ginsenoside Rg3 can effectively inhibit tumor cell proliferation, induce apoptosis of tumor cells and promote tumor necrosis in a dose-dependent manner.