地塞米松对大鼠颅脑创伤保护作用的实验研究

Experimental Study on Protective Effects of Dexamethasone on Traumatic Brain Injury in Rats

目的观察地塞米松治疗大鼠创伤性脑损伤(traumatic brain injury,TBI)后大鼠脑组织中核因子κB(NF-κB)的变化,探讨地塞米松对大鼠TBI后继发性炎症反应的影响。方法建立气体冲击致大鼠重度脑创伤模型;实验大鼠随机分为两组,脑损伤组和脑损伤十地塞米松治疗组各20只,每组又分为6h组、24h组、72h组、120h组,每组各5只;HE染色观察脑组织病理学变化;免疫组织化学检测脑组织中NF-κB水平。结果脑组织中NF-κB表达在大鼠TBI后6h即显著升高(P<0.05),伤后24h达到峰值(P<0.01),之后有所回降,但仍持续维持较高水平至120h(P<0.05);TBI大鼠经地塞米松治疗后,脑组织中NF-κB有明显降低(P<0.05)。结论地塞米松可抑制TBI大鼠脑组织中NF-κB的表达,减轻紊乱的炎性细胞因子所致的继发性损伤,起到治疗与保护作用。

Objective To investigate the changes of NF-κB in brain tissue after the treatment of naloxone in rats with traumatic brain injury, and to explore the protective effects and its mechanisms of dexamethasone on TBI. Methods The rat model of severe brain injury was produced by gas percussion. The histopathological changes of brain tissue were observed by HE stain. The expression of NF-κB in brain tissue was detected by immunohistochemical method. Results After traumatic brain injury, the expression of NF-κB in rat brain tissue significantly increased at 6 h （P〈0.05） and reached the peak value at 48 h, then the increased level of NF-κB lower down slightly and maintained at quite high level to 120 h after TBI （P 〈 0. 01）. With the treatment of dexamethasone, the expression level of NF-κB decreased significantly （P〈 0. 05）. Conclusions Dexamethasone showed protective effects by regulating the levels of NF-κB and relieved the second injury caused by the inflammatory cytokines in rat brain tissue after TBI.