摘要
目的 :研究人AK(1 3) [AngiostatinKringle (1 3) ]对大鼠C6脑胶质瘤的抑瘤效应 .方法 :利用基因转染的方法获得重组人AK(1 3)基因的C6胶质瘤细胞 ;以细胞增殖试验及免疫组化等方法检测转染细胞株是否表达了具有生物活性的人AK(1 3) .正常大鼠C6脑胶质瘤模型作对照 ,研究转染细胞株在大鼠脑内的致瘤性 .脑组织切片进行Ⅷ因子染色 .结果 :大鼠C6胶质瘤细胞稳定表达的人AK(1 3) ,在体外明显抑制牛主动脉内皮细胞的增殖 ;在体内明显抑制了大鼠C6脑胶质瘤的生长 .试验组脑切片内仅见显微瘤灶 ,Ⅷ因子染色少见新生毛细血管 .结论 :旁分泌形式作用于大鼠C6脑胶质瘤内血管内皮细胞的人AK(1 3)可明显抑制肿瘤的血管生成 。
AIM: To study the inhibition of human AK(l 3) [Angiostatin Kringle(1 3), AK(l 3)] against rat C6 glioma. METHODS: Human A(K1 3) transfected C6 cells were obtained by lipofectamine transgenosis method. Cells proliferation test and immuno histochemistry were performed to detect the angiostatin expression and its activity. The oncogenous research of the recombined C6 cell in rats was conducted compared with the normal rat C6 glioma model. The brain specimens were stained with Ⅷ factor. RESULTS: Recombined C6 cells expressed angiostatin, which inhibited the proliferation of the cattle aorta endothelial cells in vitro , and decreased the growth of the rat C6 glioma in vivo . VIII factor staining of these brain specimens only found microscopic nidus without neovascular. CONCLUSION: Human AK(i 3) against vascular endothelial cells in side secretory form can distinctly inhibit the neovascularation, which leads to the inhibition of the tumor growth.
出处
《第四军医大学学报》
北大核心
2003年第22期2041-2043,共3页
Journal of the Fourth Military Medical University
基金
国家自然科学基金资助项目 (39970 854)
