董海平+周薇+王震虹

    [摘要] 目的 探討右美托咪啶(Dex)预处理对大鼠大脑缺血再灌注(I/R)损伤后炎性反应的作用机制。 方法 72只SD大鼠随机分为6组，每组12只。①假手术组(Sham组)，大鼠经腹腔注射3%戊巴比妥钠(50 mg/kg)麻醉后，只游离右侧颈内动脉，不制作成大脑中动脉闭塞(MCAO)模型；②脑缺血组(IR组)：造模后，大鼠脑缺血90 min后再灌注；③Dex10组及Dex50组：造模后，缺血前30 min分别腹腔内注射10、50 μg/kg Dex；④Dex50+Yoh组：造模后，在给予50 μg/kg Dex前10 min腹腔内注射育亨宾(Yoh)0.5 mg/kg；⑤Yoh组：造模后，缺血前30 min腹腔注射Yoh 0.5 mg/kg。对各组大鼠进行神经功能损伤评估、梗死面积评估、肿瘤坏死因子-α(TNF-α)及白介素-1β(IL-1β)水平测定、TUNEL染色及SIRT1蛋白检测和神经运动功能评分(TMS)检测。 结果 IR组的神经功能评分、梗死面积、TUNEL(+)细胞数、TNF-a和IL-1β水平及SIRT1蛋白表达量均明显高于Sham组，再灌注后第1、2、5天时TMS评分均明显低于Sham组，差异有高度统计学意义(P 0.05)。 结论 Dex预处理可激活α2受体通过AMPK/SIRT1通路抑制大鼠脑缺血再灌注损伤，减轻炎性反应并发挥神经保护作用。

    [关键词] 右美托咪啶；炎症；再灌注损伤；脑缺血

    [中图分类号] R734 [文献标识码] A [文章编号] 1673-7210(2018)01(a)-0004-06

    [Abstract] Objective To investigate the mechanism of Dexmedetomidine (Dex) pretreatment on inflammation after cerebral ischemia/reperfusion (I/R) injury in rats. Methods Seventy-two SD rats were randomly divided into 6 groups (n=12). In sham group， after anesthesia by 3% Pentobarbital sodium (50 mg/kg)， the rates were isolated the right internal carotid artery， but they were not made into the middle cerebral artery occlusion (MCAO) model. In IR group ......