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丙酮酸乙酯通过抑制高迁移率族蛋白B1/ Toll样受体4/核因子-κB信号通路在脊髓损伤中的保护作用

Protective role of ethyl pyruvate in spinal cord injury by inhibiting the high mobility group box-1/toll-like receptor4/nuclear factor-kappa B signaling pathway.

作者信息

Fan Ruihua, Wang Lvxia, Botchway Benson O A, Zhang Yong, Liu Xuehong

机构信息

Department of Histology and Embryology, Medical College, Shaoxing University, Shaoxing, China.

School of Life Sciences, Shaoxing University, Shaoxing, China.

出版信息

Front Mol Neurosci. 2022 Sep 16;15:1013033. doi: 10.3389/fnmol.2022.1013033. eCollection 2022.

Abstract

Spinal cord injury (SCI) is a high incident rate of central nervous system disease that usually causes paralysis below the injured level. The occurrence of chronic inflammation with the axonal regeneration difficulties are the underlying barriers for the recovery of SCI patients. Current studies have paid attention to controlling the instigative and developmental process of neuro-inflammation. Ethyl pyruvate, as a derivative of pyruvate, has strong anti-inflammatory and neuroprotective functions. Herein, we reviewed the recent studies of ethyl pyruvate and high mobility group box-1 (HMGB1). We think HMGB1 that is one of the main nuclear protein mediators to cause an inflammatory response. This protein induces astrocytic activation, and promotes glial scar formation. Interestingly, ethyl pyruvate has potent inhibitory effects on HMGB1 protein, as it inhibits chronic inflammatory response by modulating the HMGB1/TLR4/NF-κB signaling pathway. This paper discusses the potential mechanism of ethyl pyruvate in inhibiting chronic inflammation after SCI. Ethyl pyruvate can be a prospective therapeutic agent for SCI.

摘要

脊髓损伤(SCI)是一种中枢神经系统疾病,发病率较高,通常会导致损伤平面以下的瘫痪。慢性炎症的发生以及轴突再生困难是脊髓损伤患者恢复的潜在障碍。目前的研究已关注于控制神经炎症的激发和发展过程。丙酮酸乙酯作为丙酮酸的衍生物,具有强大的抗炎和神经保护功能。在此,我们综述了丙酮酸乙酯和高迁移率族蛋白B1(HMGB1)的近期研究。我们认为HMGB1是引起炎症反应的主要核蛋白介质之一。这种蛋白质诱导星形胶质细胞活化,并促进胶质瘢痕形成。有趣的是,丙酮酸乙酯对HMGB1蛋白具有强大的抑制作用,因为它通过调节HMGB1/TLR4/NF-κB信号通路来抑制慢性炎症反应。本文讨论了丙酮酸乙酯抑制脊髓损伤后慢性炎症的潜在机制。丙酮酸乙酯可能是一种用于脊髓损伤的前瞻性治疗药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e5d/9524569/9ae897a3b89c/fnmol-15-1013033-g001.jpg

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