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出 处:《中华实验外科杂志》2014年第8期1697-1699,共3页Chinese Journal of Experimental Surgery
摘 要:目的 探讨瑞芬太尼在皮瓣缺血再灌注损伤中的作用及机制.方法 将80只雄性SD大鼠随机分为:假手术组(20只)、缺血再灌注(I/R)组(20只)、瑞芬太尼组(20只)、Toll样受体4(TLR4)抑制剂组(20只).制备皮瓣I/R模型.瑞芬太尼组和TLR4抑制剂组于再灌注前静脉注射瑞芬太尼1 μg/(kg· min)和E5564(5 mg/kg),分别于缺血再灌注后2、4、8h,采用实时定量聚合酶链反应(Real-time PCR)和Western blot检测TLR4和核因子-κB (NF-κB)在皮瓣组织中的表达.于术后7d,应用图像分析软件计算皮瓣存活比例.结果 Real-time PCR和Western blot检测显示I/R组比瑞芬太尼组和TLR4抑制组TLR4及NF-κB表达明显增强.瑞芬太尼组和TLR4抑制组再灌注后TLR4和NF-κB活性受到抑制.术后7dI/R组、瑞芬太尼组和TLR4抑制剂组皮瓣存活比例分别为(61.40±7.12)%、(80.31±11.63)%和(82.10±10.21)%,与I/R组比较差异有统计学意义(P<0.05).结论 瑞芬太尼可以通过抑制TLR4表达及减少NF-κB活化,减轻皮瓣缺血再灌注损伤.Objective To investigate the function and mechanism of remifentanil in flap ischemiareperfusion injury (IRI).Methods A totol of 80 adult male SD rats were randomly divided into 4 groups:sham-operated group (n =20),IRI group (n =20),remifentanil group (n =20) and Toll-like receptor 4 (TLR4) inhibitor group (n=20).Flap IRI model was established.Remifentanil group and TLR4 inhibitor group before reperfusion were intravenously injected with remifentanil 1 μg/(kg· min) and E5564 (5 mg/kg),respectively.At 2,4 and 8 h after I/R,real-time quantitative polymerase chain reaction (Real-time PCR) and Western blotting were applied to detect the expression of TLR4 and nuclear factor-κB (NF-κB) in the flap tissue.On the postoperative day 7,image analysis software was used to calculate flap survival rate.Results The Real-time PCR and Western blotting showed that the expression of TLR4 and NF-κB was significantly enhanced in IRI group as compared with remifentanil group and TLR4 inhibitor group.The expression of TLR4 and NF-κB was inhibited after reperfusion in remifentanil group and TLR4 inhibitor group.On the postoperative day 7,the flap survival rate in IRI group,remifentanil group and TLR4 inhibitor group was (61.40 ±7.12)%,(80.31 ± 11.63)% and (82.10 ± 10.21)% respectively,and there was significant difference between IRI group and remifentanil group or TLR4 inhibitor group (P < 0.05 for both).Conclusion Remifentanil may alleviate flap IRI by inhibiting TLR4 expression and activation of NF-κB.
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