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目的:探讨诱生型一氧化氮合酶抑制剂氨基胍(Aminogunidine,AG)对脑缺血-再灌流损伤保护作用的机制。方法:将大鼠随机分为对照组、AG治疗组、假手术组,测定再灌流各时相点脑内一氧化氮含量,观察光镜下顶叶皮层尼氏染色、HE染色改变。结果:再灌流不同时相点AG治疗组NO含量,顶叶皮层神经元变性程序及数量、微血管数目明显低于对照组。结论:AG可以抑制iNOS活性,降低脑内NO含量,减轻半暗带区神经元变性、微循环障碍和血脑屏障破坏,具有脑保护作用。
Objective: To investigate the protective effect of Aminogunidine (AG), an inducible nitric oxide synthase inhibitor, on cerebral ischemia-reperfusion injury in rats. Methods: The rats were randomly divided into control group, AG treatment group and sham operation group. The levels of nitric oxide in brain were measured at different time points after reperfusion. The Nissl staining of parietal cortex under light microscope was observed, and HE staining was performed. Results: The content of NO, the number of degeneration of parietal cortical neurons and the numbers of microvessels in AG-treated group at different time points after reperfusion were significantly lower than those in control group. CONCLUSION: AG can inhibit iNOS activity, decrease the content of NO in the brain, and alleviate neuronal degeneration, microcirculation and blood-brain barrier disruption in the penumbra zone and have neuroprotective effects.