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首页> 外文期刊>Mediators of inflammation >The Protective Effect of Lidocaine on Septic Rats via the Inhibition of High Mobility Group Box 1 Expression and NF-κB Activation
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The Protective Effect of Lidocaine on Septic Rats via the Inhibition of High Mobility Group Box 1 Expression and NF-κB Activation

机译:利多卡因对高迁移率族Box 1表达和NF-κB激活的抑制作用对脓毒症大鼠的保护作用

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摘要

Lidocaine, a common local anesthetic drug, has anti-inflammatory effects. It has demonstrated a protective effect in mice from septic peritonitis. However, it is unknown whether lidocaine has effects on high mobility group box 1 (HMGB1), a key mediator of inflammation. In this study, we investigated the effect of lidocaine treatment on serum HMGB1 level and HMGB1 expression in liver, lungs, kidneys, and ileum in septic rats induced by cecal ligation and puncture (CLP). We found that acute organ injury induced by CLP was mitigated by lidocaine treatment and organ function was significantly improved. The data also demonstrated that lidocaine treatment raised the survival of septic rats. Furthermore, lidocaine suppressed the level of serum HMGB1, the expression of HMGB1, and the activation of NF-κB p65 in liver, kidneys, lungs, and ileum. Taken together, these results suggest that lidocaine treatment exerts its protective effection on CLP-induced septic rats. The mechanism was relative to the inhibitory effect of lidocaine on the mRNA expression level of HMGB1 in multiple organs, release of HMGB1 to plasma, and activation of NF-κB.
机译:利多卡因是一种常见的局部麻醉药,具有抗炎作用。它已证明对败血性腹膜炎小鼠具有保护作用。然而,尚不清楚利多卡因是否对炎症的关键介质高迁移率族1(HMGB1)有影响。在这项研究中,我们调查了利多卡因治疗对盲肠结扎和穿刺(CLP)诱导的脓毒症大鼠血清HMGB1水平和肝,肺,肾和回肠中HMGB1表达的影响。我们发现利多卡因治疗可减轻CLP引起的急性器官损伤,并显着改善器官功能。数据还表明,利多卡因治疗可提高败血症大鼠的存活率。此外,利多卡因抑制肝,肾,肺和回肠中血清HMGB1的水平,HMGB1的表达以及NF-κBp65的激活。综上所述,这些结果表明利多卡因治疗对CLP诱导的脓毒症大鼠具有保护作用。其机制与利多卡因对多种器官中HMGB1 mRNA表达水平的抑制作用,HMGB1向血浆的释放以及NF-κB的活化有关。

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