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目的 NO作为中枢神经系统的信使物质和损伤状态下的氧自由基物质在脑缺血性损害中的作用非常复杂 ,研究缺血脑组织内NOS表达的变化对探讨脑缺血损害机制和脑保护十分必要。方法 大鼠大脑中动脉阻塞 (MCAO)脑缺血 /再灌注模型采用线栓法制作 ;脑组织NOS的表达采用常规NADPH d组化染色法。结果 缺血 /再灌注后脑组织神经元NADPH d染色变浅 ,阳性神经元数量减少或消失 ,而脑损伤区内NADPH d染色阳性的脑血管数量增加 ,染色加深。缺血 /再灌注 7d后NADPH d染色逐渐恢复正常。结论 缺血 /再灌注脑损伤中NO的增加可能与脑组织NADPH d表达增加有关 ,但脑组织NADPH d染色尚不能反映缺血脑组织内炎性细胞和胶质细胞NOS(主要是iNOS)表达情况 ,有必要进一步研究。
Objective NO as a messenger of the central nervous system and damage oxygen free radical substances in the role of cerebral ischemic damage is very complex to study the change of NOS expression in ischemic brain tissue to explore the mechanism of cerebral ischemia and brain protection Very necessary. Methods The cerebral ischemia / reperfusion model of middle cerebral artery occlusion (MCAO) in rats was made by thread occlusion. The expression of NOS in brain tissue was determined by routine NADPH d staining. Results NADPH d staining of neurons in the brain tissue after ischemia / reperfusion was reduced and the number of positive neurons decreased or disappeared. However, the number of NADPH d-stained brain blood vessels increased and the staining was deepened. After 7 days of ischemia / reperfusion, NADPH d staining gradually returned to normal. Conclusions The increase of NO in ischemic / reperfusion brain injury may be related to the increase of NADPH d expression in brain tissue. However, NADPH d staining of brain tissue can not reflect the expression of NOS (mainly iNOS) in inflammatory cells and glial cells in ischemic brain tissue Situation, it is necessary to further study.