纳洛酮对脑缺血大鼠海马神经元及氧自由基代谢的影响

目的探讨纳洛酮对脑缺血/再灌注损伤的防治作用及其机理。方法大鼠随机分为假手术组、脑缺血/再灌注损伤模型组、纳洛酮组和丹参组。采用四动脉结扎法建立脑缺血/再灌注损伤大鼠模型。测定脑缺血10分钟,再灌注30分钟脑组织丙二醛(MDA)浓度、超氧化物歧化酶(SOD)活性和脑组织水含量,观察海马CA1区神经元记数及病理变化。结果再灌注30分钟脑组织的MDA浓度、脑组织水含量显著增高,脑组织SOD活性及海马CA1区正常神经元记数显著降低(P<0.05和P<0.01)。使用纳洛酮后上述各指标的异常变化减轻,与再灌注组比有显著性差异(P<0.05和P<0.01)。结论纳洛酮可减轻全脑缺血/再灌注损伤,其机制与降低中枢神经元的氧自由基水平有关。

Effect of Naloxone on Hippocampal Neurons and Metabolism of Oxygen-derived Free Radidicals in Rat Cerebral Ischemia Reperfusion Injury

Objective To explore the preventive effect of Naloxone on Cerebral Ischemia Reperfusion Injury and its mechanism in rat.Methods The rats were randomized into the sham operation group,ischemia-reperfusion injury group(I/R),Naloxone-treated group and dan-shen root treated group.All rats except for those in the sham operation group were subjected to transient global ischemia using four-vessel occlusion.The reperfusion was started at 30min after 10min ischemia,then the concentration of malondialdehyde(MDA),the activity of superoxide dismutase(SOD) and the water content of the rat brain tissue were detected,then the count and the pathological change of neurons in hippocampal CA1 were studied.Results The concentration of MDA and water content of the brain tissues increased remarkably and the superoxide dismutase(SOD) reduced significantly;the count of normal neurons in Hippocampi CA1 decreased significantly and neuron injured noticeably in ischemia-reperfusion injury group(P<0.05 and P<0.01).In Naloxone-treating group,the indexes of abnormal changes mentioned above were improved markedly,and there was significant difference between I/R group and Naloxone group(P <0.05 and P<0.01).Conclusion Naloxone could improve the brain ischemia-reperfusion injury,its mechanism may relate to the decreased oxygen free radicals level.