威麦宁抗小鼠Lewis肺癌转移作用及分子机制的研究

目的: 探讨威麦宁抗小鼠Lewis肺癌转移作用及其分子机制。方法: 接种Lewis肺癌细胞复制移植性肺癌转移模型,用药后计数肺表面转移灶的数目;免疫组化法检测瘤组织中血管内皮细胞CD34的表达情况、并计数微血管密度(MVD)和瘤细胞表面E-cadherin蛋白表达率;RT-PCR法检测瘤细胞E-cadherin mRNA的表达水平。结果: NS(生理盐水组)、WL(威麦宁低剂量组)、WH(威麦宁高剂量组)、CTX(环磷酰胺组)各组肺转移灶发生率依次为100%、90%、60%和40%。瘤组织内MVD计数, WH组MVD明显低于NS组(P<0.01)。WH组瘤细胞膜表面E-cadherin蛋白表达率及E-cadherin mRNA水平明显高于NS组(P<0.01)。 结论: 威麦宁可能通过提高瘤细胞E-cadherin mRNA及E-cadherin蛋白的表达;减少瘤组织微血管形成等机制,发挥抗Lewis肺癌荷瘤小鼠移植性肺转移作用。

The molecular mechanism of inhibition of murine Lewis lung carcinoma metastasis by weimaining in vivo

AIM: To investigate the anti-metastasis effect of weimaining, extracted from fragopyrum cymosum meissn, a Chinese medicine, on murine Lewis lung carcinoma (3LL). METHODS: The anti-metastasis effect of weimaining in vivo was detected in the grafting lung metastasis model of murine Lewis lung carcinoma. The effects of the drug on the expression of CD34 and E-cadherin were investigated by immunohistochemical staining and RT-PCR. RESULTS: Weimaining effectively inhibited the lung metastasis of 3LL at a concentration of 250 mg·kg^-1·d^-1, significantly suppressed the expression of CD34 and increased the expression levels of E-cadherin protein and mRNA in 3LL cells. CONCLUSIONS: Weimaining inhibits the metastasis of murine Lewis lung carcinoma (3LL) in vivo via increasing the expression of E-cadherin and decreasing microvessel density of tumor tissue.