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目的探讨内毒素预处理对大鼠前脑缺血再灌注后脑组织诱生型一氧化氮合酶(iNOS),神经型一氧化氮合酶(nNOS)的影响及意义。方法采用大鼠全脑缺血再灌注模型,动态观察大脑皮层、海马、小脑组织中iNOS、nNOS的活性及海马CA1区神经元计数的变化。结果脑缺血再灌注后大脑皮层、海马、小脑组织中iNOS和nNOS活性均显著高于正常对照组,缺血前24 h经尾静脉注入内毒素衍化物MPL(20 g/kg)可明显降低再灌注大脑皮层、海马、小脑组织中iN-OS、nNOS的活性和海马CA1区神经元计数下降幅度。结论提示脑缺血再灌注后,大脑皮层、海马、小脑组织中iNOS、nNOS活性发生了明显变化,内毒素预处理显著抑制了缺血再灌注后脑组织中iNOS、nNOS的活性。
Objective To investigate the effect and significance of endotoxin preconditioning on inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS) in brain tissue after forebrain ischemia-reperfusion in rats. Methods The global cerebral ischemia / reperfusion model was used to observe the changes of iNOS and nNOS activity and neuron count in the hippocampal CA1 area in the cerebral cortex, hippocampus and cerebellum. Results The activity of iNOS and nNOS in cerebral cortex, hippocampus and cerebellum after cerebral ischemia and reperfusion were significantly higher than those in normal control group. The MPL (20 g / kg) injected into caudal vein 24 h before ischemia decreased significantly The activity of iN-OS and nNOS in the cerebral cortex, hippocampus and cerebellum after reperfusion and the decrease of neuron count in CA1 area of hippocampus were observed. The results suggest that iNOS and nNOS activity in cerebral cortex, hippocampus and cerebellum change significantly after cerebral ischemia-reperfusion, and endotoxin preconditioning can significantly inhibit the activity of iNOS and nNOS in brain tissue after ischemia-reperfusion.