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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.
Fan, Ruihua; Wang, Lvxia; Botchway, Benson O A; Zhang, Yong; Liu, Xuehong.
Afiliação
  • Fan R; Department of Histology and Embryology, Medical College, Shaoxing University, Shaoxing, China.
  • Wang L; School of Life Sciences, Shaoxing University, Shaoxing, China.
  • Botchway BOA; Department of Histology and Embryology, Medical College, Shaoxing University, Shaoxing, China.
  • Zhang Y; School of Life Sciences, Shaoxing University, Shaoxing, China.
  • Liu X; Institute of Neuroscience, Zhejiang University School of Medicine, Hangzhou, China.
Front Mol Neurosci ; 15: 1013033, 2022.
Article em En | MEDLINE | ID: mdl-36187352
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.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2022 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2022 Tipo de documento: Article