地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Experimental investigation on protective effect of dexamethasone therapy to traumatic brain injury in rats

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.