摘要
目的外伤性脑损伤后促炎细胞因子释放增多,并引起脑损伤。文中观察β2肾上腺素能受体(简称β2受体)阻断剂ICI 118551对外伤性脑损伤大鼠促炎细胞因子释放的影响,并研究其是否具有脑保护作用。方法成年雄性SD大鼠18只,随机均分为3组(n=6):假手术组(S组)、外伤性脑损伤组(T组)及ICI 118551治疗组(I组)。T组和I组分别静脉注射等容等渗盐水或ICI 118551 20 mg/kg,20 min后建立外伤性脑损伤模型。6 h后抽血检测各组大鼠血清肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-6(interleukin-6,IL-6)及神经元特异性烯醇化酶(neuronespecificenolase,NSE)水平。结果与S组相比,T组及I组TNF-α、IL-6和NSE水平升高(P<0.05);与T组相比,I组TNF-α、IL-6和NSE水平降低(P<0.05)。结论β2受体阻断剂ICI 118551具有脑保护作用,这可能与抑制外伤性脑损伤后炎症反应有关。
Objective Proinflammatory cytokines increase after traumatic brain injury （TBI） and result in brain damage. Recent studies suggest that β2-adrenoceptor antagonist can reduce proinflammatory cytokines. This study aims to observe the effects of β2-adrenoceptor antagonist ICI 118551 on proinflammatory cytokine release and to investigate whether ICI 118551 has neuroprotective effect. Methods Eighteen Sprague-Dawley male rats were equally randomized into a sham-operation group, a TBI group and an ICI 118551 treatment group, the latter two injected intravenously with equal volume of normal saline and ICI 118551 at 20 mg/kg, respec- tively, and the TBI model was established 20 rain later. Blood samples were obtained 6 h after TBI for the determination of the levels of tumor necrosis factor-alpha （TNF-α）, Interleukin-6 （IL-6） and neuronespecificenolase （NSE）. Results The levels of TNF-α, IL-6 and NSE were significantly increased in the TBI and ICI 118551 groups as compared with the sham-operation group （P 〈 0.05 ）,but remarkably decreased in the ICI 118551 group in comparison with the TBI group （ P 〈 0. 05 ）. Conclusion 132-adrenoceptor antagonist ICI 118551 has the brain-protecting effect, which may be attributed to the inhibition of inflammatory reactions after TBI.
出处
《医学研究生学报》
CAS
北大核心
2012年第2期140-142,共3页
Journal of Medical Postgraduates
