肾缺血-再灌注后大鼠肾组织一氧化氮的代谢研究  

Study on Metabolism of Renal Nitric Oxide in Rat with Renal Ischemia-reperfusion

作　　者：王新良[1] 陈晓玲[2] 王佩薇[1] 谢菲[1] 黄善生[2] 

机构地区：[1]河北医科大学第二附属医院儿科,石家庄050000 [2]河北医科大学第二附属医院病理生理教研室,石家庄050000

出　　处：《昆明医学院学报》2005年第3期59-63,共5页Journal of Kunming Medical College

摘　　要：目的:探讨肾I-R后大鼠肾组织NO的代谢.方法:建立大鼠肾I-R模型,用硝酸还原酶法测定NO含量,SP试剂盒免疫组织化学法检测肾组织cNOS、iNOS蛋白定位表达,Western blot检测肾组织cNOS、iNOS蛋白半定量表达.结果:(1)肾I-R后大鼠肾脏NO代谢异常,入肾血、出肾血NO2-/NO3-含量增多;同时肾组织NO2-/NO3-含量和尿液NO2-/NO3-排出率也有增高(P<0.05);(2)肾I-R后大鼠肾组织cNOS表达增多,以I-R1 h最明显;iNOS则在I-R5 h表达增多;(3)I-R1 h和I-R5 h大鼠肾小球内cNOS阳性信号均明显增强;而肾小管内cNOS阳性信号I-R1 h显著减弱;I-R1 h可见髓袢升枝和降枝粗段的肾小管有微弱的iNOS表达,而I-R5 h肾小管的iNOS阳性信号明显增强.结论:肾I-R导致了大鼠肾脏cNOS、iNOS蛋白表达改变,从而使NO代谢异常.Objective： To investigate metabolism of renal nitric oxide in rat with renal ischemia- reper- fusion. Methods： In the rat model of renal ischemia - reperfusion, NO^2-/ NO^3- was determined by nitrate reductase and renal cNOS protein was detected by ABC immunohistochemistry and Western blot. Results： （ 1 ） Metabolism of renal nitric oxide was Abnormal in rat with renal ischemia - reperfusion： the NO^2 -/NO^3 - content of IRB, ORB was remarkably increased （P 〈 0.01）, meanwhile the NO^2-/NO^3- content of kidney and urine also increased （P 〈0.05）. （2） Expression of cNOS was strengthened especially in I-R1 h, but the iNOS signal was stronger in I- R5 h rats. （3） 140 kDa cNOS protein appeared in the kidney of sham. For I - R1 h and I - R5 h rats, I - R1 h was the most distinctive, next was I - R5 h. There was no 135 kDa iNOS protein in sham, a little in I - R1 h, a great deal in I - R5 h. Conclusion： cNOS and iNOS proteins were changed in renal I - R rats, which results in the abnormal of NO metabolism.

关 键 词：肾 缺血再灌注 一氧化氮 CNOS INOS 大鼠 

分 类 号：R692.5[医药卫生—泌尿科学]