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机构地区:[1]重庆医科大学基础医学院病理教研室,重庆400016
出 处:《重庆医科大学学报》2004年第4期437-440,共4页Journal of Chongqing Medical University
摘 要:目的 :研究Genistein对人卵巢浆液性乳头状囊腺癌细胞系SKOV3 诱导人内皮细胞系ECV - 30 4迁移的作用 ,以探讨Genistein抑制血管生成作用的机理。方法 :采用微孔滤膜培养小室及双室联合细胞培养方法 ,观察在 0 .5 %BS培养条件下 ,SKOV3 细胞或其条件培养基诱导的ECV - 30 4细胞迁移以及Genistein对SKOV3 细胞或其条件培养基诱导的ECV - 30 4细胞迁移的影响 ;用免疫组化方法检测血管生长因子VEGF、bFGF及TGFβ - 1蛋白的表达水平。 结果 :SKOV3 细胞或其条件培养基对内皮细胞均有较强的趋化作用 ,Genistein对SKOV3 细胞或其条件培养基诱导的ECV - 30 4细胞迁移有呈剂量依赖性的抑制作用。 2 0 μmol/LGenistein处理ECV - 30 4细胞 4 8h后 ,VEGF、bFGF蛋白的表达水平降低 ,而TGFβ - 1蛋白的表达水平升高。结论 :Genistein可明显抑制人卵巢浆液性乳头状囊腺癌细胞系SKOV3 及其条件培养基对人内皮细胞系ECV- 30 4细胞的诱导迁移作用 ;Genistein可能通过抑制促血管生成调节因子VEGF和bFGF的蛋白表达 ,增强血管生成的负性调节因子TGFβ -Objective:To investigate the effect of Genistein on migration of human endothelial cells ECV-304 induced by human ovarian serous cystadenocarcinoma cell line SKOV_3,and to explore the mechanism of anti-angiogenesis of Genistein.Methods:Millicell chamber and coculture method were used to observe the influence on migration of ECV-304 induced by SKOV_3 cells or its conditioned media,and the effect of Genistein on migration of ECV-304 induced by SKOV_3 cells or its conditioned media without serum.The expression of angiogenesis associated protein VEGF,bFGF and TGFβ-1 were determined using immunocytochemical method.Results:Either SKOV_3 cells or its conditioned media could induce the committed chemotactic migration of ECV-304.The chemotactic migrations of ECV-304 induced by SKOV_3 or its conditioned media were significantly inhibited by Genistein in a dose-dependent manner.20μmol/L Genistein could down-regulate the expression of VEGF and bFGF;up-regulate the expression of TGFβ-1.Conclusion:Migrations of ECV-304 induced by human ovarian carcinoma cell line SKOV_3 or its conditioned media were apparently inhibited by Genistein.It suggests that this inhibitory effect of Genistein is completed by down-regulating the expression of vessel growth-promoting factor VEGF and bFGF,and up-regulating the expression of negative regulator TGFβ-1.This may be one of the mechanisms of anti-angiogenesis of Genistein.
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