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利多卡因的分子机制。

Molecular mechanisms of lidocaine.

作者信息

Karnina Resiana, Arif Syafri Kamsul, Hatta Mochammad, Bukhari Agussalim

机构信息

Doctoral Program of Biomedical Sciences, Faculty of Medicine, Hasanuddin University, Makassar, Sulawesi Selatan, Indonesia.

Faculty of Medicine, Muhammadiyah University of Jakarta, Banten, Indonesia.

出版信息

Ann Med Surg (Lond). 2021 Aug 17;69:102733. doi: 10.1016/j.amsu.2021.102733. eCollection 2021 Sep.

DOI:10.1016/j.amsu.2021.102733
PMID:34457261
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8379473/
Abstract

Lidocaine is an amide-class local anesthetic used clinically to inhibit pain sensations. Systemic administration of lidocaine has antinociceptive, antiarrhythmic, anti-inflammatory, and antithrombotic effects. Lidocaine exerts these effects under both acute and chronic pain conditions and acute respiratory distress syndrome through mechanisms that can be independent of its primary mechanism of action, sodium channel inhibition. Here we review the pathophysiological underpinnings of lidocaine's role as an anti-nociceptive, anti-inflammatory mediated by toll-like receptor (TLR) and nuclear factor kappa-β (NF-kβ) signalling pathways and downstream cytokine effectors high mobility group box 1 (HMGB1) and tumour necrosis factor-α (TNF-α).

摘要

利多卡因是一种临床上用于抑制痛觉的酰胺类局部麻醉剂。利多卡因的全身给药具有抗伤害感受、抗心律失常、抗炎和抗血栓形成作用。利多卡因在急性和慢性疼痛状态以及急性呼吸窘迫综合征中,通过与其主要作用机制(钠通道抑制)无关的机制发挥这些作用。在此,我们综述了利多卡因作为抗伤害感受、抗炎介质的病理生理学基础,其作用是由Toll样受体(TLR)和核因子κ-β(NF-κβ)信号通路以及下游细胞因子效应物高迁移率族蛋白B1(HMGB1)和肿瘤坏死因子-α(TNF-α)介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c6/8379473/332cec658d90/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c6/8379473/6395bca2b79b/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c6/8379473/198d4350160b/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c6/8379473/332cec658d90/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c6/8379473/6395bca2b79b/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c6/8379473/198d4350160b/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c6/8379473/332cec658d90/gr3.jpg

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