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    冷诱导 RNA 结合蛋白在心跳骤停心肺复苏后脑损伤中的作用*

    Effects of CIRP on cardiac arrest/cardiopulmonaryresuscitation-induced brain ischemia/reperfusion injury

    • 摘要: 目的 探究心跳骤停心肺复苏后大鼠海马 CIRP 的表达变化,探讨其在心跳骤停心肺复苏后脑损伤中作用机制。方法 健康成年雄性 Sprague Dawley(SD)大鼠 36 只,采用随机数字表法均分成两组(n=18):Sham 组(S 组)和缺血再灌注 48h 组(I/R48h 组)。Sham 组只给予气管插管和动静脉穿刺,不给予电刺激;I/R 48h组大鼠气管插管和动静脉穿刺后,经食管电刺激诱发室颤建立心跳骤停模型。复苏 后48 小时,行神经功能评分 ;苏木精-伊红染色(hematoxylin and eosin staining, HE)观察海马 CA1 区锥体细胞形态改变;免疫组化法检测海马中小胶质细胞特异性标志抗体Iba-1 的表达;Western blot检测海马组织 CIRP 总蛋白和浆蛋白表达。结果 与Sham组相比,复苏后 48 小时的神经功能评分明显降低(P<0.05);海马 CA1 区神经元死亡数目明显增多(P<0.05);海马 CA1 区 Iba-1 表达增加 (P<0.05);海马组织中 CIRP 总蛋白和浆蛋白表达明显增加(P<0.05)。结论 心跳骤停心肺复苏可诱导 CIRP 的高表达,CIRP 可从细胞核移位到细胞胞浆中,CIRP 可能参与大鼠心脏骤停心肺复苏后脑组织损伤的早期炎症反应过程。

       

      Abstract: Objective To investigate the expression of cold-inducible RNA binding protein(CIRP) in the rats hippocampus after cardiopulmonary resuscitation (CPR). The possible role of CIRP in cardiac arrest/cardiopulmonary resuscitation(CA/CPR)-induced brain ischemia/reperfus injury in rats was investigated in this study.Methods 36 adult male Sprague Dawley (SD) rats were randomly divided into two groups using a random number table (n=18): sham group and ischemia-reperfusion 48h(I/R48h) group.Sham group was given tracheal intubation and arteriovenous puncture only and no electrical stimulation was given.I/R 48h group were given tracheal intubation and arteriovenous puncture ,then establishment of cardiac arrest model induced by transesophageal electricalstimulation induced ventricular fibrillation . At 48h after return of spontaneous circulation (ROSC), neurodeficit Score (NDS) was evaluated ;neuronal death was analyzed by hematoxylin and eosin (H&E);microglialactivation was evaluated by detecting the expression of ionized calcium-binding adaptermolecule-1(Iba-1) by immunohistochemistry ;the expression of CIRP in the hippocampus were determined by Western blot.Results The neurological function score was better in sham-operated rats than those that were underwent CA/CPR(P<0.05);the neuronal death were enhanced in the hippocampus CA1 region of three I/R48h group as compared with those in the sham-operated group (P<0.05);microglia were activated theneuronal death was aggravated in the hippocampus CA1 region of mice subjected to I/R48h group as compared with those in t he sham-operated group (P<0.05);the expression level of total protein and cytoplasm protein of CIRP in the hippocampus were significantly increased in the hippocampus in I/R48h group compare to sham group(P<0.05).Conclusions CA/CPR can induce high expression of CIRP ,CIRP can run from the nucleus to thecytoplasm,cirp may be involved in the early inflammatory reaction process of braintissue damage after CA/CPR in rats

       

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