人参皂甙Rg3抗小鼠Lewis肺癌的机制研究

目的以小鼠Lewis肺癌为肿瘤模型探讨人参皂甙Rg3抗肿瘤机制。方法以肺癌细胞系LLC荷瘤C57/BL小鼠建立小鼠肺癌模型,随机分为人参皂甙Rg3组、阳性药顺铂组和模型组,分别给予人参皂甙Rg3、顺铂和生理盐水;同时设立空白对照组。以肿瘤质量、抑瘤率观察人参皂甙Rg3的抗肿瘤效果;以流式细胞术测定脾脏CD4+T细胞、CD8+T细胞数量及比值;以Elispot技术检测机体肿瘤抗原特异性CTL的诱生情况;以肝脏指数、脾脏指数、胸腺指数判定人参皂甙Rg3的毒副作用。结果人参皂甙Rg3组抑瘤率高于顺铂组,差异具有统计学意义(P<0.05)。生理盐水组小鼠脾脏CD4+T细胞、CD8+T细胞百分率比正常小鼠低,而人参皂甙Rg3组和顺铂组高于生理盐水组,差异具有统计学意义(P<0.05)。人参皂甙Rg3组肿瘤特异性IFN-γ斑点数明显增多,与生理盐水组相比具有统计学差异(P<0.05),顺铂组脾脏无肿瘤特异性IFN-γ斑点出现。和模型组相比较,人参皂甙Rg3组小鼠肝脏、脾脏、胸腺指数无明显差异,而顺铂组的肝脏、脾脏、胸腺指数低于人参皂甙Rg3组,差异具有统计学意义(P<0.05)。结论 LLC细胞荷瘤小鼠具有明显的免疫抑制现象,人参皂甙Rg3可显著增加脾脏CD4+T细胞、CD8+T细胞阳性率并促进肿瘤特异性CTL细胞诱生,人参皂甙Rg3无肝脏、胸腺、脾脏毒性。

The anti-tumor mechanism of Ginsenoside Rg3 in murine Lewis lung carcinoma model

To investigate antitumor mechanisms and toxicity of ginsenoside Rg3,C57BL/6 mice implanted with Lewis lung cancer cells were further administrated with ginsenoside Rg3,cisplatinum,and physiological saline water respectively.Then the antitumor effect,mechanisms and toxicity were determined by tumor inhibition rate,flow cytometry,Elispot and organ index respectively.The results showed that tumor inhibition rates of cisplatinum and ginsenoside Rg3 groups were 20.77% and 47.88%,respectively.Tumor implantation could decrease CD4+ T and CD8+ T percentages of splenocytes from(20.60±1.196)% and(13.36±0.926)% to(11.79±0.3256)% and(6.278±0.263)%,respectively.Both ginsenoside Rg3 and cisplatinum administrations could reverse the decrease of CD4+ T and CD8+ T cells induced by tumor implantation.Contrast to physiological saline water,ginsenoside Rg3 could obviously increase IFN-γ spots number from 4.000±0.3162 to 11.40±3.487,while cisplatinum administration could not achieve any IFN-γ spots.Importantly,cisplatinum administration induced obvious toxicities and result in decreased indexes of liver,spleen and thymus,while the ginsenoside Rg3 treatment did not.All the results suggested that ginsenoside Rg3,which had no obviously liver,spleen and thymus toxicity effects,could obviously inhibit LLC tumor formation by enhancing both CD4+ T and CD8+ T cell percentages and promoting tumor specific CTL priming.