甘草甜素对缺血/再灌注损伤器官的保护机制及研究进展

摘要

缺血/再灌注损伤是临床常见的病理现象，严重的缺血/再灌注损伤可引起全身炎症反应综合征，甚至多器官功能障碍综合征。高迁移率族蛋白B1( HMGB1)作为一种早期炎性因子参与缺血/再灌注损伤，抗HMGB1治疗可以减轻组织缺血/再灌注损伤程度。甘草甜素可以与HMBG1结合并抑制其炎性因子作用，减轻缺血/再灌注损伤，该文综述了HMGB1的结构、释放、受体及转导通路、功能及甘草甜素对缺血/再灌注损伤器官的保护作用及可能机制和研究进展。%Ischemia/reperfusion injury is a common clinical pathology,severe ischemia/reperfusion inju-ry can cause systemic inflammatory response syndrome,multiple organ dysfunction syndrome even. High-mob-ility group protein B1 ( HMGB1 ) acts as an early mediator of inflammation in ischemia-reperfusion injury. glycyrrhizin is known to bind to HMGB1 directly,resulting in inhibition of proinflammatory cytokine-like ac-tivity of this protein, ameliorates I/R-Induced Injury. This paper reviews the structure, release, receptors, pathways,functions of HMGB1,and progress in the protective effect and the possible mechanism of glycyrrhi-zin.