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转染人Angiostatin K(1-3)基因的C_6细胞在大鼠脑内的致瘤性研究

Oncogenous researches of the human angiostatin K(1-3) gene transfected C_6 cells in Wistar rat
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摘要 目的 研究人AngiostatinK(1 3 )IAK(1 3 )I对大鼠C6脑胶质瘤的抑瘤效应。方法 构建真核表达载体 pcDNA3 SAK(1 3 ) ,用脂质体法导入C6细胞后 ,与正常C6细胞对照 ,分别接种于Wistar大鼠脑内 ,进行生存期及脑内瘤灶大小的比较 ,脑标本行苏木素 伊红 (HE)及Ⅷ因子血管染色。结果 接种转基因C6细胞的大鼠脑内无肉眼可见的瘤灶 ,其生存期明显长于接种正常C6细胞的大鼠 (P <0 .0 1) ,HE及Ⅷ因子染色只可见显微大小的无血管瘤灶。结论 旁分泌形式作用于瘤内血管内皮细胞的人AK (1 3 ) ,可明显抑制瘤内血管生成 ,进而抑制肿瘤生长。 Objective To study the inhibitory effect of human angiostatin K(1 3) against C 6 glioma.Methods The eukaryotic expression vector pcDNA3 SA(K1 3) containing human angiostatin(K1 3)cDNA was established,then transfected into C 6 cells with lipofectamine.Transfected C 6 cells and normal C 6 cells were transplanted into the brains of Wistar rats respectively to observe the life cycle of the rats and the growth of the tumors.HE and Ⅷ factor staining of the brain specimens were also carried out.Results No gross tumor loci were observed in the brains of the rats transfected with C 6 cells and the life cycle of these rats was much longer than controls(P<0.01).HE and Ⅷ factor staining of these brain specimens only showed microscopic nidus without vessels.Conclusion Human AK(1 3) against vascular endothelial cells in side secretion form could distinctly inhibit the neovascularation,leading to the inhibition of the tumor growth.
出处 《中华实验外科杂志》 CAS CSCD 北大核心 2002年第4期369-370,共2页 Chinese Journal of Experimental Surgery
基金 国家自然科学基金资助项目 (39970 854)
关键词 致瘤性 ANGIOSTATIN 旁分泌细胞交流 C6胶质瘤细胞 脑肿瘤 大鼠 基因转染 Angiostatin Paracrine communication C 6 glioma
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