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目的:探讨核因子-κB(nuclearfactor-κB,NF-κB)在缺血再灌注大鼠海马神经元中的表达及纳洛酮的影响。方法:用插线法制作大鼠大脑中动脉闭塞(middlecerebralarteryocclusion,MCAO)局灶性脑缺血再灌注模型,海马区NF-κBP65亚单位的水平通过免疫组化来测定,苏木精-伊红染色观察缺血侧脑组织形态学变化。结果:缺血再灌注组大鼠缺血侧海马区P65亚单位的表达较假手术组显著增强(P<0.01),给予纳洛酮处理后,P65的表达减弱(P<0.01)。缺血再灌注组缺血侧海马区许多神经元有凋亡现象,缺血再灌注纳洛酮组凋亡神经元减少,假手术组未见凋亡神经元。结论:短暂的脑缺血可导致海马区NF-κB的表达增加,凋亡神经元增多。海马区NF-κB的激活与神经元的凋亡相关,纳洛酮可抑制海马区NF-κB的表达,减少神经元的凋亡。
Objective: To investigate the expression of nuclear factor-κB (NF-κB) in hippocampal neurons during ischemia-reperfusion in rats and the effect of naloxone. Methods: The middle cerebral artery occlusion (MCAO) model of focal cerebral ischemia-reperfusion in rats was made by the method of patch-line. The level of NF-κB P65 subunit in hippocampus was determined by immunohistochemistry. The expression of hematoxylin-eosin Morphological changes of ischemic brain tissue were observed by staining. Results: The expression of P65 subunit in ischemic hippocampus of ischemia-reperfusion group was significantly higher than that of sham operation group (P <0.01). The expression of P65 decreased after naloxone treatment (P <0.01). A number of neurons in the ischemic hippocampal region of ischemia-reperfusion group showed apoptotic phenomenon. Apoptotic neurons of Naloxone group were decreased after ischemia-reperfusion and no apoptotic neurons were observed in sham-operation group. CONCLUSION: Short-term cerebral ischemia can result in an increase of NF-κB expression and increase of apoptotic neurons in hippocampus. The activation of NF-κB in hippocampus is related to neuronal apoptosis. Naloxone can inhibit the expression of NF-κB in hippocampus and decrease the apoptosis of neurons.