尹婉约1 , 何 治1,2,*
1三峡大学基础医学院,宜昌 443002 2肿瘤微环境与免疫治疗湖北省重点实验室(三峡大学),宜昌 443002

摘 要:

高迁移率族蛋白1 (high mobility group box-1, HMGB1) 是一种含有215 个氨基酸残基的核蛋白,几乎存在于所有真核细胞中,参与调节染色体结构、基因转录、DNA 复制和修复等多项生理过程,在生长发育过程中发挥着重要作用。越来越多的研究结果显示,HMGB1 通过多种途径参与细胞凋亡、自噬和炎症反应等多种病理生理过程,从而诱导脑缺血再灌注(cerebral ischemia-reperfusion, CIR) 损伤。此外,目前发现存在多种物质能靶向抑制HMGB1 的表达,进而发挥抗炎、抗细胞凋亡和抗氧化损伤等作用,但具体作用机制仍需更加深入的研究。进一步挖掘和探索HMGB1 在CIR 损伤中的具体作用及其相关抑制剂将为CIR 损伤的临床治疗提供新的潜在候选策略和思路。因此,本文就HMGB1 在CIR 损伤过程中的作用及其相关抑制剂的研究进展作一简要综述。

通讯作者:何 治 ,

Advancement on the role of HMGB1 in the process of cerebral ischemia-reperfusion injury and its related inhibitors
YIN Wan-Yue1 , HE Zhi1,2,*
1College of Basic Medical Science, China Three Gorges University, Yichang 443002, China 2Hubei Key Laboratory of Tumor Microenvironment and Immunotherapy, China Three Gorges University, Yichang 443002, China


High mobility group box-1 (HMGB1) is a nuclear protein containing 215 amino acid residues, which exists in almost all eukaryotic cells. It can participate in various physiological processes such as chromosome structure regulation, gene transcription, DNA replication and repair, thus playing an important role in growth and development. An increasing number of research results indicate that HMGB1 participates in various pathological and physiological processes such as cell apoptosis, autophagy, and inflammatory response through multiple pathways, thereby inducing cerebral ischemia-reperfusion (CIR) injury. In addition, it has been found that multiple substances can target to inhibit HMGB1 expression, to exert anti-inflammatory, anti-apoptotic, and antioxidant effects. However, the specific mechanism of action still requires more in-depth study. Further excavation and exploration of the specific role of HMGB1 in CIR injury and its related inhibitors will provide new potential candidate strategies and ideas for the clinical treatment of CIR injury. Therefore, this article provides a brief review on the role of HMGB1 in the process of CIR injury and the research progress of its related inhibitors.

Communication Author:HE Zhi ,

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