军事医学2017，Vol.41Issue(12)：956-961,6.DOI:10.7644/j.issn.1674-9960.2017.12.003
炎症因子在缺血再灌注大鼠海马各亚区表达研究
Expression of inflammatory factors in hippocampal subregions of rats after cerebral ischemia-reperfusion
摘要
Abstract
Objective To detect the damage of hippocampal neurons and the changes in inflammatory cytokines in rats after cerebral ischemia-reperfusion(I/R)and compare the expressions of IL-1β,IL-6 and TNFαin hippocampal DG,CA1 and CA3 subregions.Methods The focal cerebral I/R model was induced by an intraluminal filament embolism.The SD rats were randomly divided into the sham-operated group(SHAM group)and the middle cerebral artery occlusion-reperfusion group(MCAO group).HE staining was employed to detect the damage to hippocampal DG, CA1 and CA3 subregions.The expression levels of IL-1β, IL-6 and TNFα were detected by immunofluorescence assay.Results Compared with SHAM group,hippocampal DG,CA1 and CA3 subregion neurons in MCAO group were severely damaged, with occurred inflammatory cell infiltration,and a large amount of neurons apoptosis, and the expressions of IL-1β, IL-6 and TNFαin each subregion increased significantly.At the same time, in MCAO group, the expression of inflammatory cytokines in CA1 subregion was more significant than that in DG and CA 3 subregions(P<0.05).Conclusion Cerebral I/R could cause neuronal damage, inflammatory cell infiltration, and neuronal apoptosis in the DG, CA1 and CA3 subregions of the hippocampus and increase the release of inflammatory cytokines.In MCAO group, the expression of inflammatory cytokines in CA1 subregion of hippocampus is significantly higher than that in DG and CA 3 subregions, suggesting that CA1 region is more sensitive to I/R injury.关键词
缺血再灌注/海马亚区/炎症因子/炎性细胞浸润/白细胞介素1β/白细胞介素6/肿瘤坏死因子αKey words
ischemia-reperfusion/hippocampus subregion/inflammatory factor/inflammatory cell infiltration/interleu-kin-1 beta/interleukin-6/tumor necrosis factor-alpha分类
医药卫生引用本文复制引用
程曼,刘朝琦,董志萍,王梦影,杨柳,张绪梅..炎症因子在缺血再灌注大鼠海马各亚区表达研究[J].军事医学,2017,41(12):956-961,6.基金项目
国家自然科学基金资助项目(81373003) （81373003）
