瑞芬太尼对小鼠脑缺血再灌注损伤的神经保护作用

Neural protection of Remifentanil on cerebral ischemia reperfusion injury of mice

目的观察瑞芬太尼对小鼠脑缺血再灌注损伤后神经功能障碍及梗死灶体积的影响。方法线栓法制备大脑中动脉阻塞的脑缺血再灌注模型。96只雄性小鼠随机分为假手术组、模型组和瑞芬太尼预处理组。再灌注24 h后进行神经功能缺陷评分,氧化三苯甲基四氮唑(TTC)染色测定梗死面积,酶联免疫吸附法(ELISA)检测缺血侧大脑皮层组织中白细胞介素(IL)-1β、肿瘤坏死因子(TNF)-α、IL-10和转化生长因子(TGF)-β1的含量,并用蛋白免疫印迹法检测缺血侧大脑皮层组织中核转录因子κB(NF-κB)的活性。结果瑞芬太尼能明显改善小鼠的神经行为,缩小梗死面积,抑制促炎症因子IL-1β和TNF-α的表达,而增加抗炎症因子IL-10和TGF-β1的表达,并抑制NF-κB的活化。结论瑞芬太尼对小鼠脑缺血再灌注损伤具有明显的保护作用,其机制与抵抗炎症反应有关。

Objective To investigate the protective effects of remifentanil on cerebral ischemia reperfusion injury in mice.Methods Transient focal cerebral ischemia was induced by middle cerebral artery occlusion.96 male mice were randomly divided into sham opera-tion, model, remifentanil groups.24 h after reperfusion , the neurological deficit score and infarction area were measured.The levels of IL-1β, TNF-α, IL-10 and TGF-β1 in the ischemic cortex were measured by ELISA.At the same time , the NF-κB expression was also exam-ined by Western Blot.Results Remifentanil ameliorated neurological dysfunctions and reduced infarction volume.Moreover, treatment with remifentanil reduced the expression of pro-inflammatory cytokines IL-1βand TNF-α, and up-regulated the expression of anti-inflammatory cy-tokines IL-10 and TGF-β1 in the ischemic brain.In addiction , activation of NF-κB was inhibited by cordycepin treatment.Conclusions Remifentanil affords strong neuroprotective effect against cerebral ischemia reperfusion injury .The anti-inflammatory effects of remifentanil may be involved in the protective mechanism.