出 处:《World Journal of Gastroenterology》2004年第22期3361-3364,共4页世界胃肠病学杂志(英文版)
基 金:Supported by the Key Technologies Research and Development Program of Heilongjiang Province During the 9th Five-Year Plan Period,No.G99C 19-5
摘 要:AIM:To investigate the antiangiogenic effects of endostatin on colonic carcinoma cell line implanted in nude mice and its mechanism. METHODS:Nude mice underwent subcutaneous injection with LS-174t colonic carcinoma cell line to generate carcinoma and were randomly separated into two groups.Mice received injection of vehicle or endostatin every day for two weeks. After the tumor was harvested,the tumor volumes were determined,and the expressions of CD34,VEGF and FIk-1 were examined by immunohistochemical method. RESULTS:Tumor volume was significantly inhibited in the endostatin group(84.17%)and tumor weight was significantly inhibited in the endostatin group(0.197±0.049) compared to the control group(1.198±0.105)(F=22.56, P=0.001),microvessel density(MVD)was significantly decreased in the treated group(31.857±3.515)compared to the control group(100.143±4.290)(F=151.62,P<0.001). Furthermore,the expression of FIk-1 was significantly inhibited in the treated group(34.29%) ompared to the control group(8.57%)(X^2=13.745,P=0.001).However no significant decrease was observed in the expression of vascular endothelial growth factor(VEGF)between these two groups(X^2=0.119,P=0.730). CONCLUSION:Endostatin can inhibit tumor growth and angiogenesis by blocking Vegf/FIk-1 pathway.This experiment provides the theory basis for developing a new anti-carcinoma drug through studying the properties of anti-angiogenesis inhibitors.AIM: To investigate the antiangiogenic effects of endostatin on colonic carcinoma cell line implanted in nude mice and its mechanism. METHODS: Nude mice underwent subcutaneous injection with LS-174t colonic carcinoma cell line to generate carcinoma and were randomly separated into two groups. Mice received injection of vehicle or endostatin every day for two weeks. After the tumor was harvested, the tumor volumes were determined, and the expressions of CD34, VEGF and FIk-1 were examined by immunohistochemical method. RESULTS: Tumor volume was significantly inhibited in the endostatin group (84.17%) and tumor weight was significantly inhibited in the endostatin group (0.197±0.049) compared to the control group (1.198±0.105) (F=22.56, P=0.001), microvessel density (MVD) was significantly decreased in the treated group (31.857±3.515) compared to the control group (100.143±4.290) (F=151.62, P<0.001). Furthermore, the expression of FIk-1 was significantly inhibited in the treated group (34.29%) compared to the control group (8.57%) (x^2=13.745, P=0.001). However no significant decrease was observed in the expression of vascular endothelial growth factor (VEGF) between these two groups (x^2=0.119, P=0.730). CONCLUSION: Endostatin can inhibit tumor growth and angiogenesis by blocking Vegf/FIk-1 pathway. This experiment provides the theory basis for developing a new anti-carcinoma drug through studying the properties of anti-angiogenesis inhibitors.
关 键 词:Angiogenesis Inhibitors Animals Antigens CD34 Cell Line Tumor Colonic Neoplasms ENDOSTATINS MICE Mice Nude Neovascularization Pathologic Research Support Non-U.S. Gov't Vascular Endothelial Growth Factor A Vascular Endothelial Growth Factor Receptor-2 Xenograft Model Antitumor Assays
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