【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.更多还原

【Abstract】 Objective: To investigate metabolism of renal nitric oxide in rat with renal ischemia-reperfusion.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 IR1?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.更多还原