【摘要】 目的研究盐酸右美托咪定对心肌缺血-再灌注损伤大鼠心肌组织中Toll样受体(toll-like receptor,TLR)-4mRNA、核因子(nuclear factor,NF)-κB mRNA的表达,探讨盐酸右美托咪定对心肌缺血-再灌注损伤大鼠心肌TLR-4/NF-κB信号通路的影响。方法健康3个月龄SD雄性大鼠21只,体重250~300g,随机均分为三组:假手术组(sham组)、缺血-再灌注组(IR组)、缺血-再灌注+盐酸右美托咪定组(DEX组)。采用结扎左冠状动脉前降支的方法制备大鼠心肌缺血-再灌注损伤模型,sham组左冠状动脉穿线不结扎。Sham组和IR组在结扎前30min经腹腔注射生理盐水100μg/kg,DEX组在结扎前30min经腹腔注射盐酸右美托咪定注射液100μg/kg(4μg/ml)。实时定量逆转录聚合酶链反应(RT-PCR)方法检测TLR-4mRNA和NF-κB mRNA的表达。结果sham、IR和DEX组的TRL-4mRNA分别为(2.21±0.11)、(7.83±0.35)和(3.91±0.21),sham、IR和DEX组的NF-κB mRNA分别为(0.013±0.166)、(0.051±0.016)和(0.015±0.004),IR、DEX组的TRL-4mRNA和NF-κB mRNA的表达明显高于sham组,且DEX组TRL-4mRNA和NF-κB mRNA的表达明显低于IR组(P<0.05)。结论盐酸右美托咪定可降低缺血-再灌注损伤大鼠心肌组织TLR-4mRNA和NF-κBmRNA的表达,盐酸右美托咪定可以调控TLR/NF-κB信号通路的转导,抑制炎症反应,减轻心肌缺血-再灌注损伤,保护心肌。更多还原

【Abstract】 Objective To investigate the influence of dexmedetomidine on expression of TLR-4 and NF-κB mRNA in rats with myocardial ischemia/reperfusion injury(IR).Methods Twenty-one healthy Sprague-Dawley male rats,weighing 250-300g,were randomly divided into 3groups:group sham,group IR,and IR +Dexmedetomidine group(group DEX).Left anterior descending coronary artery was ligatured to establish myocardial IR model.100μg/kg dexmedotomidine was administered intraperitoneally 30 ming before ligature in grouop DEX,while the same volume of saline was administered in groups sham and IR.The expression of myocardial TLR-4mRNA and NF-κB mRNA were determined by real-time fluorescence quantitative(RT-PCR).Results The TLR-4mRNA and NF-κB mRNA expression was significantly higher in groups IR and DEX compared with group sham(P<0.05).Compared with group IR,TLR-4mRNA and NF-κB mRNA decreased in group DEX(P <0.05).Conclusion Dexmedetomidine can reduce systemic inflammatory response,so that to protect myocardial ischemia/reperfusion injury through regulating TLR4/NF-κB signal pathway.更多还原