NO增加兔局灶脑缺血后缺血脑组织VEGF表达  

NO upgrades expression of VEGF protein and mRNA in local ischemic brain tissues of rabbits

作　　者：田恒力[1] 周良辅[1] 崔宇辉[2] 陈浩[2] 

机构地区：[1]复旦大学附属华山医院神经外科,上海200040 [2]上海交通大学附属第六人民医院神经外科,上海200233

出　　处：《中风与神经疾病杂志》2006年第5期588-590,共3页Journal of Apoplexy and Nervous Diseases

基　　金：上海市科学技术委员会资助项目(03ZR14059)

摘　　要：目的一氧化氮(NO)和血管内皮生长因子(VEGF)参与血管再生并且可能在脑缺血相互影响,本实验探讨NO对局灶脑缺血后VEGF表达的影响。方法兔局灶脑缺血后应用NO合成底物:左旋-精氨酸(L-Arg),荧光RT-PCR分析缺血脑组织VEGF mRNA表达,ELISA分析VEGF蛋白,脑组织含水率评价脑水肿。结果L-Arg明显增加缺血区VEGF蛋白(1.180±0.433ng/ml vs0.649±0.274ng/ml,P<0.05)和mRNA表达(0.3402±8.876×10-3vs0.2025±0.0413,P<0.05),同时减轻脑水肿(P<0.01)。结论外源性NO增加缺血区VEGF表达,减轻脑水肿,提示联合应用NO合成底物和VEGF对脑缺血后神经保护可能起到更好的协同作用。Objective No and VEGF may mediate angiogenesis and interact to promote angiogenesis in an ischemic brain. The aim of the study as to investigate the effects of exogenous NO on VEGF expression. Methods NO donor,L-arginine was intravenously administered to rabbits daily after cerebral ischemia. The expression of VEGF protein was assessed by ELISA. Flurosecent RT-PCR was carried out to estimate the mRNA levels of VEGF. Brain edema was determined by measuring brain water content. Results Compared to control groups,L-arginine significantly enhanced VEGF protein levels(1.180±0.433ng/ml vs 0.649±0.274ng/ml,P< 0.05 ) and VEGF mRNA expression(0.3402±8.876×10~ -3 vs 0.2025±0.0413,P< 0.05 ) in ischemic brain tissue,and diminished water levels of ischemic brain tissue. Conclusion The findings that exogenous NO enhances VEGF expression of ischemic brain tissue and alleviates brain edema suggest combination treatment with NO donor and VEGF may have synergistic effects on neuroprotection after cerebral ischemia.

关 键 词：脑缺血 一氧化氮 左旋-精氨酸 血管内皮生长因子 

分 类 号：R743.3[医药卫生—神经病学与精神病学]