反应停调控Lewis肺癌表达bFGF和MMP-2

Mechanism study of thalidomide regulating angiogenesis in Lewis lung cancr model

目的 探讨反应停抑制Lewis肺癌血管形成的机制。方法 采用Lewis肺癌模型和免疫组化方法探讨反应停抑制肺癌生长的机制。结果 反应停剂量为 2 0 0、4 0 0mg/kg时 ,对Lewis肺癌的生长有抑制作用 ,对微血管密度 (microvesseldensity ,MVD)、碱性成纤维细胞生长因子 (bFGF)及基质金属蛋白酶 2 (MMP 2 )的表达有下调作用 (P <0 .0 5 )。结论 反应停可能通过抑制促进血管生长的因子bFGF和MMP 2的表达 ,抑制了血管生成 ,并进一步抑制了Lewis肺癌的生长。

Objective To investigete the mechanism of thalidomide regulating angiogenesis in Lewis lung cancer model. Methods Mice model of Lewis lung cancer was established, treated with different doses of thalidomide。Normal saline and TNP470 were as negative and positive factor。 Masses of tumor were weighed。 bFGF and MMP-2 , MVD were evaluated by CD34 antibody with immunohistochemistry, the level of bFGF and MMP-2 was examined by Western Blot method. Results Thalidomide(200 or 400 mg/kg)inhibitd the growth of Lewis lung cancer, down regulated the expression of bFGF and MMP-2, and reduced MVD in Lewis lung cancer model. Conclusion Thalidomide can inhibit the angiogenesis inhibiting vascular growth factors bFGF and MMP-2 in Lewis lung cancer.