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地塞米松对脑损伤大鼠核转录因子-κB水平的影响
引用本文:杜晓冬,李国平,叶磊,刘鹏,曹钰.地塞米松对脑损伤大鼠核转录因子-κB水平的影响[J].中国危重病急救医学,2009,21(1):364-366,385.
作者姓名:杜晓冬  李国平  叶磊  刘鹏  曹钰
作者单位:四川大学华西医院急诊,四川成都,610041;
摘    要:Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.

关 键 词:脑创伤    地塞米松    炎症反应    核转录因子-κB    nuclear  factor-κB    

Experimental investigation on protective effect of dexamethasone therapy to traumatic brain injury in rats
Abstract:
Keywords:traumatic brain injurydexamethasoneinflammatory response
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