摘要
目的:探讨星形胶质细胞在局灶脑缺血/再灌注后炎症反应中的作用。方法:健康雄性Wistar大鼠,随机分为正常对照组、假手术组、模型组、吡咯烷二硫基甲酸酯(PDTC)干预组、生理盐水组,采用大脑中动脉线栓法制备局灶脑缺血/再灌注模型,结合HE染色、原位杂交、免疫组化、荧光免疫组化双标,观察缺血侧星形胶质细胞的变化以及NF-κB p65、ICAM-1在星形胶质细胞的表达。结果:局灶脑缺血/再灌注24 h脑梗死面积最大,PDTC干预组脑梗死面积明显减少;模型组抗小鼠胶原纤维酸性蛋白(GFAP)和2种炎性介质的表达都强于其它组(P<0.05),PDTC干预组GFAP和2种炎性介质的表达均低于模型组(P<0.05)。结论:局灶脑缺血/再灌注早期有大量反应性星形胶质细胞出现在缺血区并表达NF-κB p65、ICAM-1,可能启动炎症级联反应,影响其它神经细胞的继发反应。
Objective： To explore the effects of astrocyte in an inflammatory reaction of focal cerebral ischemia / reperfusion. Methods： Healthy male Wistar rats were randomly divided into normal control group,sham-operation group,model group,PDTC intervention group and saline group. Right middle cerebral artery was occluded by string embolus to establish a focal cerebral ischemia / reperfusion model,HE stain,fluorescence in situ hybridization（ FISH）,immunohistochemistry,double-labelling immunofluorescence were used to observe the changes of astrocytes in ischemic lesion and the expression of NF-κB p65,ICAM-1 in astrocytes. Results： The largest focal cerebral ischemia / reperfusion area appeared at 24 hours after ischemia / reperfusion but with an obvious decrease in PDTC intervention group. In model group,expression of glial fibrillary acidic protein（ GFAP） and two inflammatory mediators were significantly up-regulated compared with other groups（ P〈0. 05）. In PDTC intervention group,expression of GFAP and two inflammatory mediators were dramatically lower than those of the other groups（ P〈0. 05）. Conclusions： A large amount of astrocytes appear in ischemic lesion after early focal cerebral ischemia / reperfusion and express NF-κB p65,ICAM-1,which may elicited the inflammatory cascade and secondary injury of other nerve cells.
出处
《内科急危重症杂志》
2016年第3期219-224,共6页
Journal of Critical Care In Internal Medicine
