ADMA/DDAH通路在脑缺血再灌注致肺微血管内皮细胞损伤中的作用  

The role of ADMA/DDAH pathway in pulmonary microvascular endothelial cells injury induced by cerebral ischemia and reperfusion

作　　者：吴云虎[1] 王殿华[2] 

机构地区：[1]安徽中医学院第一附属医院脑病中心,安徽合肥230031 [2]昆明医科大学,云南昆明650031

出　　处：《中风与神经疾病杂志》2013年第10期898-901,共4页Journal of Apoplexy and Nervous Diseases

基　　金：广西壮族自治区自然基金项目(2011GXNSFA013280)

摘　　要：目的探索ADMA/DDAH通路在脑缺血再灌注损伤(I/R)致急性肺损伤(ALI)大鼠肺微血管内皮细胞(PMVECs)损伤中的作用。方法培养大鼠PMVECs,采用大鼠脑缺血再灌注损伤后2h的血清干预4h后,MTT比色试验检测细胞活力,Western blot和RT-PCR技术检测PMVECs中的PKC、MLCK蛋白及其mRNA的表达。结果 ADMA干预后PMVECs生长受限,ADMA不仅使细胞活力降低,而且使PKC和MLCK蛋白的表达增强,同时上调PKC和MLCK mRNA的表达,但是ADMA的降解酶DDAH能显著抑制PMVECs的这些变化。结论在ADMA/DDAH通路中ADMA与DDAH通过调控PKC和MLCK的表达参与大鼠PMVECs损伤,ADMA/DDAH通路在脑I/R致肺微血管内皮细胞损伤过程中扮演重要角色。Objective To explore the role of ADMA/DDAH pathway in acute lung injury （ALI） induced by cere- bral ischemia repeffusion injury （I/R） in pulmonary microvascular endothelial cells （PMVECs） in rats. Method Cul- tured rat PMVECs. Serum made from two hours cerebral isehemia and reperfusion injury intervented PMVECs. After four hours, checking viability of cell detected by MTF method ; Expression of PKC and MLCK protein and mRNA in lung detected by method of western blot and RT-PCR. Result Morphology of cell changed significantly after intervented by ADMA ;AD- MA not only made the viability of cell reduce, but also enhanced expression of PKC and MLCK protein, at the same time, in- creased expression of PKC and MLCK mRNA （P 〈 0.05 ） , but DDAH inhibited these changes significantly in PMVECs （P 〈 0.05）. Conclusion Some material such as ADMA and DDAH in ADMA/DDAH pathway caused PMVECs damage in rat, ADMA/DDAH pathway plays an important role in process of acute lung injury induced by brain I/R.

关 键 词：ADMA DDAH通路 缺血再灌注 急性肺损伤 肺微血管内皮细胞 

分 类 号：R743.3[医药卫生—神经病学与精神病学]