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首页> 外文期刊>Resuscitation. >Differential effect of resuscitation on Toll-like receptors in a model of hemorrhagic shock without a septic challenge.
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Differential effect of resuscitation on Toll-like receptors in a model of hemorrhagic shock without a septic challenge.

机译：在没有脓毒症挑战的失血性休克模型中，复苏对Toll样受体的不同作用。

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It has been shown that the inflammatory response and cellular damage after hemorrhagic shock are influenced by resuscitation strategies. Toll-like receptors (TLRs) play an important role in signal transduction in inflammatory conditions. However, alterations in TLR expression following hemorrhagic shock and resuscitation have not been well documented. This study was conducted to measure the impact of different resuscitation strategies on TLR expression and downstream signaling in key organs. METHODS: Sprague Dawley rats (n=38) were subjected to a severe volume-controlled hemorrhage protocol. After 75 min of shock, they were resuscitated over 45 min as follows: (1) lactated Ringer's (LR, 81 ml/kg), (2) ketone Ringer's (KR, 81 ml/kg), (3) 7.5% hypertonic saline (HTS, 9.7 ml/kg), (4) 6% hetastarch (HEX, 27 ml/kg), (5) pyruvate Ringer's (PR, 81 ml/kg). Sham hemorrhage (NH) and no resuscitation (NR) groups served as controls. The KR and PR solutions were identical to LR except for equimolar substitution of racemic lactate with beta hydroxybutyrate and sodium pyruvate, respectively. At the end of resuscitation, the expression of TLRs (types 1-10), and cytokines (IL-10, IL-1beta and TNF-alpha) were measured in the lung and spleen using RT-PCR. Levels of phosphorylated and total IkB-alpha and NF-kappaB were detected by Western blotting. The systemic and lung protein levels of TNF-alpha were measured using ELISA and immunohistochemistry. RESULTS: Expression of TLRs in the lung was affected more than in the spleen by hemorrhagic shock and resuscitation. In the lung, hemorrhage increased TLR-2, -3 and -6 (but not TLR-4) mRNA expression, with an up-regulation of the ratio of phosphor-NF-kappaBp65 and total NF-kappaBp65, NF-kappaBp65 activation, and enhanced systemic and tissue TNF-alpha protein levels. Post-resuscitation, TLR mRNA profile and subsequent downstream proteins in the lung and spleen were affected by the choice of resuscitation strategy. CONCLUSIONS: Hemorrhagic shock activates TLR signaling in lung, but not the spleen, probably through an up-regulation of TLR gene expression, and activation of NF-kappaB pathway. Resuscitation modulates this response in a fluid- and tissue-specific fashion.
机译：已经表明，失血性休克后的炎症反应和细胞损伤受复苏策略的影响。 Toll样受体（TLR）在炎症条件下的信号转导中起重要作用。但是，出血性休克和复苏后TLR表达的改变尚未得到充分记录。进行这项研究以测量不同复苏策略对关键器官中TLR表达和下游信号传导的影响。方法：Sprague Dawley大鼠（n = 38）接受严格的体积控制性出血方案。休克75分钟后，按以下步骤在45分钟内复苏：（1）乳酸林格氏液（LR，81 ml / kg），（2）酮林格氏液（KR，81 ml / kg），（3）7.5％高渗盐水（HTS，9.7毫升/千克），（4）6％苦味酒（HEX，27毫升/千克），（5）丙酮酸林格氏液（PR，81毫升/千克）。假出血（NH）组和无复苏（NR）组作为对照组。 KR和PR溶液与LR相同，除了分别用β羟基丁酸酯和丙酮酸钠等摩尔取代外消旋乳酸酯。复苏结束时，使用RT-PCR测量肺和脾中TLRs（1-10型）和细胞因子（IL-10，IL-1beta和TNF-α）的表达。通过Western印迹检测磷酸化的和总的IkB-α和NF-κB的水平。使用ELISA和免疫组化方法检测TNF-α的全身和肺蛋白水平。结果：失血性休克和复苏对肺部TLRs的影响比对脾脏的影响更大。在肺部，出血增加了TLR-2，-3和-6（但不是TLR-4）的mRNA表达，并且上调了磷-NF-kappaBp65和总NF-kappaBp65，NF-kappaBp65的比率，以及增强了全身和组织中的TNF-α蛋白水平。复苏策略的选择会影响复苏后，TLR mRNA谱以及随后的肺和脾中下游蛋白的表达。结论：失血性休克可能通过上调TLR基因表达并激活NF-κB通路激活肺部TLR信号，但不激活脾脏。复苏以流体和组织特异性方式调节该反应。

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