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利多卡因通过抑制高迁移率族蛋白 B1 表达和 NF-κB 激活对脓毒症大鼠的保护作用。

The protective effect of lidocaine on septic rats via the inhibition of high mobility group box 1 expression and NF-κB activation.

机构信息

Department of Anesthesiology, Qilu Hospital, Shandong University, No. 107 Wenhuaxi Road, Jinan, Shandong 250012, China.

Department of Cardiology, Qilu Hospital, Shandong University, No. 107 Wenhuaxi Road, Jinan, Shandong 250012, China.

出版信息

Mediators Inflamm. 2013;2013:570370. doi: 10.1155/2013/570370. Epub 2013 Nov 25.

Abstract

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.

摘要

利多卡因是一种常见的局部麻醉药物,具有抗炎作用。它已被证明在脓毒症性腹膜炎的小鼠模型中具有保护作用。然而,目前尚不清楚利多卡因是否对高迁移率族蛋白 B1(HMGB1)具有影响,HMGB1 是炎症的关键介质。在这项研究中,我们研究了利多卡因治疗对盲肠结扎穿孔(CLP)诱导的脓毒症大鼠血清 HMGB1 水平和肝脏、肺脏、肾脏和回肠中 HMGB1 表达的影响。我们发现,CLP 引起的急性器官损伤被利多卡因治疗减轻,器官功能得到显著改善。数据还表明,利多卡因治疗提高了脓毒症大鼠的存活率。此外,利多卡因抑制了血清 HMGB1 水平、HMGB1 表达以及肝脏、肾脏、肺脏和回肠中 NF-κB p65 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。其机制与利多卡因抑制多个器官中 HMGB1 的 mRNA 表达水平、HMGB1 向血浆中的释放以及 NF-κB 的激活有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed15/3858876/5a5931befd90/MI2013-570370.001.jpg

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