摘要
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 study the expression of NF κB in cerebral ischemia reperfusion in rat and the protective action of naloxone. Methods:Focal ischemia reperfusion model was prepared in adult male rats by left middle cerebral artery occlusion (MCAO). The expression of NF κB P65 subunit in ischemic hippocampus was determined by immunocytochemistry and the histological evidence of focal ischemia reperfusion was demonstrated by means of hematoxylin eosin stained. Results:The nuclear immunostaining for NF κB P65 was stronger in the ischemia reperfusion group than that in the ischemia reperfusion naloxone group,while NF κB localization was not observed by immunocytochemistry in sham operated control group.The neurons in hippocampus had histological evidence of apoptosis in ischemia reperfusion group.Histological evidence of apoptosis was also observed in ischemia reperfusion naloxone group, but less intensely.No evidence of apoptosis could be observed in sham-operated control group. Conclusion:Transient ischemia resulted in a marked activation of nuclear NF κB and notable evidence of apoptosis in the neurons in hippocampus.The activation of NF κB was associated with apoptosis of neurons. The results suggest that naloxone may inhibit neuronal apoptosis by preventing the activation of NF κB.
出处
《南京医科大学学报（自然科学版）》
CAS
CSCD
北大核心
2002年第6期479-480,499,F002,共4页
Journal of Nanjing Medical University(Natural Sciences)
