摘要
【目的】探讨右旋美托咪啶在脑缺血再灌注损伤中的保护作用和相关机制。【方法】42只雄性SD大鼠随机分为3组,每组14只:右旋美托咪啶组(Dex)采用右旋美托咪啶5μg·kg-1·h-1恒速输注2 h;拮抗剂组(Dex+Yoh)于开启注射泵前10 min经尾静脉输注拮抗剂育亨宾1 mg/kg,余用法同上组;对照组(Con)以同等速度输注生理盐水2 h。所有大鼠行大脑中动脉栓塞术,缺血90 min后再灌注。观察术后24 h神经功能评分、脑梗死体积、水肿指数以及脑组织白介素(IL)-1β、肿瘤坏死因子(TNF)-α水平、核蛋白NF-κB p65表达量。【结果】再灌注24 h后,脑梗死体积的比较显示Dex组(17±2.8)%较Dex+Yoh组(38±4.9)%与Con组(42±5.7)%明显减小(P<0.05),水肿指数比较显示Dex组(1.021±0.098)较Dex+Yoh组(1.342±0.137)与Con组(1.417±0.105)显著降低,差异有统计学意义(P<0.05)。脑组织IL-1β、TNF-α及NF-κB p65蛋白表达量的比较均显示Dex组较Dex+Yoh组与Con组明显下降(P<0.05)。【结论】右旋美托咪啶通过抑制NF-κB通路的激活减少促炎因子的产生,对大鼠局灶性脑缺血再灌注损伤具有保护作用。
[Objective] To investigate the protective effect and mechanism of dexmedetomidine on the brain ischemic-reperfusion injury in rat.[Methods] Male Sprague-Dawley rats weighing 270-300 g were randomly divided into three groups （n =14 each group）：（1）dexmedetomidine group （Group Dex） received dexmedetomidine administration at a rate of 5 μg/kg/h for 2 h,（2） antagonist group （Group Dex＋Yoh） was given yohimbine 1 mg/kg 10 min before the same dexmedetomidine administration as Group Dex and （3）control group （Group Con） received 0.9% sodium chloride at a corresponding rate as placebo.All rats were subjected to right middle cerebral arterial occlusion （MCAO） for 90 min.After allowing reperfusion for 24 h,the cerebral infarction volume,edema index and neurological scores were measured,the levels of interleukin （IL）-1β,tumor necrosis factor （TNF）-α and the expression of nuclear NF-κB p65 in brain tissue were evaluated.[Results] After brain reperfusion for 24 hours,the infarction volume of Group Dex （17 ± 2.8）% was significantly lower than that of Group Dex＋Yoh （38 ± 4.9）% and Group Con （42 ± 5.7）% （P〈 0.05）,the edema index in Group Dex （1.021 ± 0.098） was decreased than that in Group Dex＋Yoh （1.342 ± 0.137） and Group Con （1.417 ± 0.105,P 〈 0.05）.Simultaneously,compared with Group Dex＋Yoh or Group Con,the tissue levels of IL-1β,TNF-α,and the expression of nuclear NF-κB p65 were significantly reduced in Group Dex （all P 〈 0.05）.[Conclusions] Dexmedetomidine can attenuate brain ischemic-reperfusion injury in rats partly through inhibiting the activation of NF-κB and suppressing the overexpression of pro-inflammatory factors.
出处
《中山大学学报（医学科学版）》
CAS
CSCD
北大核心
2013年第6期851-855,共5页
Journal of Sun Yat-Sen University:Medical Sciences
基金
广东省科技计划项目(2010B031600206
2010B060900030)
关键词
右旋美托咪啶
脑
缺血再灌注
大鼠
dexmedetomidine
brain
ischemia/reperfusion injury
rat
