人参皂苷Rg3联合紫杉醇抗胃癌转移的作用及机制研究

Experiment Study of Gisenoside Rg3 and Paclitaxel on inhibiting Gastric Cancer Cells' Metastasis and Its Mechanism

目的:探讨人参皂苷Rg3联合紫杉醇协同抗胃癌转移的作用及机制。方法:将人胃癌BGC—823细胞裸鼠移植瘤动物模型,随机分为四组(每组10只):人参皂苷Rg3组[GS-Rg3:10mg/(kg.d)灌胃]),紫杉醇组(10 mg/kg腹腔内注入,每周二次),联合组(人参皂苷Rg3+紫杉醇,用法同上),对照组(生理盐水组)。连续用药3周。用药结束后脱颈处死裸鼠,统计各组转移率,免疫组化检测微血管密度(MVD),RT-PCR测定血管生成因子β3-整合素的mRNA水平。结果:联合组肿瘤转移率低于紫杉醇组和人参皂苷Rg3组(P<0.05,P<0.01),联合组肿瘤微血管密度(MVD)最低,与人参皂苷Rg3组和紫杉醇组比较有显著差异(P<0.05和P<0.01),联合组β3-整合素最低,与紫杉醇组、人参皂苷Rg3组比较均有显著差异(P<0.05,P<0.01).结论:人参皂苷Rg3联合紫杉醇具有协同抗胃癌转移作用,可能通过协同抑制肿瘤新生血管形成有关。

Objective：To explore inhibiting Gastric cancer Cells＇ Metastasis and Its Mechanism of Gisenoside Rg3 and Paclitaxel.Methods： Transplantation tumor models of gastric cancer cells BGC-823 in SCID mice were randomly divided into four groups（10 mice per group）： Ginsenoside Rg3 group（GS-Rg3： 10mg/Kg/d intragastric administration,for three weeks）,Paclitaxel group（Paclitaxel at 10mg/Kg was injected into abdominal cavity two times per week,for three weeks）,the combined group（GS-Rg3＋ Paclitaxel,using the same method above）.After medication was over,every group of mice were decapitated,cancer metastasis ratesand inhibition rates were tested;immunohistochemistry was to detect microvessel density（MVD）;RT-PCR was to detect mRNA expression of β3-integrin.Result： Tumor metastasis rate of the combined group was lower than GS-Rg3 group and Paclitaxel group（P0.05,P0.01）;MVD in the combined group was the lowest and there was significant statistical difference contrast to GS-Rg3 or Paclitaxel group（P0.05 or P0.01）;β3-integrin expression in the combined group was the lowest and there was significant statistical difference comparing with Paclitaxel or GS-Rg3 group（P0.05,P0.01）.Conclusion： Combined group could inhibit tumors＇ Metastasis and its mechanism may be correlated with Collaborative inhibiting tumor neovascularity.