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目的:探讨人参皂苷Rg3对肺腺癌小鼠移植瘤生长和转移的抑制作用及其可能的机制。方法:接种Lewis细胞构建高转移肺腺癌小鼠移植瘤模型,随机分为对照组(0.9%氯化钠溶液)、顺铂(cisplatin,DDP)组和人参皂苷Rg3组;肿瘤细胞接种后4d给予相应药物干预,接种后24d处死小鼠,剥离皮下肿瘤并取出肺组织,计算抑瘤率和肺表面结节转移抑制率;应用免疫组织化学法检测移植瘤组织中生长抑素受体(somatostatin receptor,SSTR)、血管内皮生长因子(vascular endothelial growth factor,VEGF)和增殖细胞核抗原(proliferation cell nuclear antigen,PCNA)的表达水平,TUNEL法检测移植瘤中肿瘤细胞的凋亡情况。结果:DDP组和人参皂苷Rg3组的抑瘤率分别为39.20%和54.86%(P<0.01)。DDP组和人参皂苷Rg3组的肺表面结节转移抑制率分别为30.25%和58.57%,差异有统计学意义(P<0.05)。人参皂苷Rg3组中SSTR的表达水平和肿瘤细胞凋亡指数高于对照组和DDP组(P<0.01),人参皂苷Rg3组中VEGF的表达水平和PCNA增殖指数低于对照组和DDP组(P<0.01,P<0.05)。结论:人参皂苷Rg3对肺腺癌小鼠移植瘤的生长和转移具有明显抑制作用,其机制可能与SSTR的过表达有关。
Objective: To investigate the inhibitory effect of ginsenoside Rg3 on the growth and metastasis of lung adenocarcinoma mouse xenografts and its possible mechanism. Methods: Lewis lung carcinoma cells were transplanted into BALB / c mice with high metastatic lung adenocarcinoma and were randomly divided into control group (0.9% sodium chloride solution), cisplatin (DDP) group and ginsenoside Rg3 group. The mice were sacrificed 24 days after inoculation, the subcutaneous tumor was dissected and the lung tissues were removed to calculate the tumor inhibition rate and inhibition rate of pulmonary nodular metastasis. Immunohistochemistry was used to detect somatostatin (SSTR), vascular endothelial growth factor (VEGF) and proliferating cell nuclear antigen (PCNA) were detected by flow cytometry. TUNEL assay was used to detect the apoptosis of tumor cells. Results: The inhibitory rates of DDP and ginsenoside Rg3 were 39.20% and 54.86% (P <0.01). The inhibitory rates of pulmonary nodular metastasis in the DDP group and the ginsenoside Rg3 group were 30.25% and 58.57%, respectively, with statistical significance (P <0.05). The expression level of SSTR and the apoptosis index of tumor cells in ginsenoside Rg3 group were higher than those in control group and DDP group (P <0.01). The expression of VEGF and PCNA in ginsenoside Rg3 group were lower than those in control group and DDP group <0.01, P <0.05). CONCLUSION: Ginsenoside Rg3 has a significant inhibitory effect on the growth and metastasis of lung adenocarcinoma xenografts in mice, which may be related to the overexpression of SSTR.