摘要
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 determine the effects and significance of endotoxin preconditioning on iNOS activity, nNOS activity in rat cerebral cortex, hippocampus and cerebella region after global brain ischemia/reperfusion. Methods Global ischemia for 20 min was made by four-vessel occlusion model （4-vo） in 60 Wistar rats, among which 30 were injected of 20 μg/kg MPL through caudal vein 24 h before model establishment. Another 8 rats undergoing sham operation served as controls. The dynamic change of iNOS activity, nNOS activity and neuron density of the cerebral cortex, hippocampus and cerebella region were observed at 1, 4, 8 h after reperfusion. Results The activity of iNOS and nNOS decreased significantly after endotoxin preconditioning in the regions mentioned above, as compared with that of rats only undergoing the ischemia/reperfusion. The neuron number in rat hippocampus decreased after ischemia/reperfusion, but no significant difference was found between control and endotoxin preconditioning groups. Conclusion The activity of iNOS and nNOS changed significantly after global brain ischemia/reperfusion. That endotoxin preconditioning decreased iNOS and nNOS activities may be the protective mechanism.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2006年第13期1404-1406,共3页
Journal of Third Military Medical University
关键词
脑缺血
预处理
内毒素
一氧化氮
cerebral ischemia
precohditioning
endotoxin
NOS
