• 大鼠局灶脑缺血/再灌注星形胶质细胞的反应和NF-κBp65、ICAM-1在星形胶质细胞中的表达
  • Astrocytes’ reaction in rats with focal cerebral ischemia/reperfusion and expression of NF -κB p65, ICAM-1 in astrocytesYin Yan*1, Yixue Gu*2, Duo Liu1, Guibo Feng#3
  • 颜因.大鼠局灶脑缺血/再灌注星形胶质细胞的反应和NF-κBp65、ICAM-1在星形胶质细胞中的表达[J].内科急危重症杂志,2016,22(3):
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    中文关键词:  星形胶质细胞  局灶脑缺血/再灌注  炎症反应 NF-κB p65 ICAM-1
    英文关键词:astrocyte, focal  cerebral ischemia/reperfusion, inflammatory  reaction, NF-κB  p65, ICAM-1
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    作者单位E-mail
    颜因 重庆市第九人民医院神经内科 yanyinyy00@126.com 
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    中文摘要:
          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、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24h脑梗死面积最大,PDTC干预组脑梗死面积明显减少;模型组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/再灌注后早期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。
    英文摘要:
          Objective:To discuss effects of astrocyte in an inflammatory reaction of focal cerebral ischemia/secondary perfusion. Method: Healthy, male Wistar rats, were randomly divided into a normal control group, Sham-operated group, model group, PDTC intervention group, anda saline group. We took middle cerebral artery occlusion to make a focal cerebral ischemia/reperfusion model, combinedit with HE staining,Sfluorescence in situ hybridization(FISH), immunohistochemistry, double-labelling immunofluorescence to observe changes of astrocytes in ischemic lesion and expression of NF -κB p65, ICAM 1 in astrocytes. Results: The largest focal cerebral ischemia/reperfusion area is at twenty four hours with an obvious decrease in PDTC intervention group. In model group, expression of GFAP and two inflammatory mediators wereSsignificantly up-regulated compared with other groups (p<0.05), In PDTC intervention group, expression of GFAP and two inflammatory mediators wereSSdramaticallySlower than thatSin other groupsS(P<0.05). Conclusion: A large amount of astrocyte appeared in ischemic lesion after early focal cerebral ischemia/reperfusion and express NF-κB p65, ICAM-1, which may start inflammatory cascade reactions and secondarily affect other nerve cells.