摘要
目的探讨地塞米松对大鼠重度创伤性颅脑损伤(TBI)后脑组织中核转录因子-κB(NF-κB)的影响。方法将Wistar大鼠随机分为TBI组和地塞米松治疗组,采用气体冲击致大鼠重度TBI模型。各组于术后0、6、24、72、120h取5只大鼠活杀,取脑组织,苏木素-伊红(HE)染色观察脑组织病理学变化。免疫组化检测脑组织中NF-κB水平。结果TBI后6h大鼠脑组织中NF-κB表达即显著升高(P〈0.05),于伤后24h达峰值(P〈0.01),之后有所回降,至120h仍维持较高水平(P〈0.05或P〈0.01)。经地塞米松治疗后6、24、72h脑组织中NF-κB显著低于TBI组(P均〈0.01)。结论大鼠TBI后早期脑组织中NF-κB即反应性升高,并维持较高水平,引起炎症级联反应,导致TBI后继发性损伤。地塞米松可抑制NF-κB,减轻紊乱的炎症细胞因子所致的继发性损伤,起到治疗与保护作用。
Objective To explore the effects of dexamethasone on nuclear factor-κB (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. 0l). 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.
出处
《中国危重病急救医学》
CAS
CSCD
北大核心
2009年第6期364-366,I0001,共4页
Chinese Critical Care Medicine
基金
四川省科技重点项目(06kjt-15)
关键词
脑创伤
地塞米松
炎症反应
核转录因子-ΚB
traumatic brain injury
dexamethasone
inflammatory response
nuclear factor-κB