CAJ | 학술논문

背景心肌缺血/再灌注损伤(myocardial ischemia/reperfusion,MI/RI)的发生机制主要与氧化应激损伤有关,补充外源性的锌对心肌进行预处理,能够保护缺血/再灌注损伤的心肌,但具体机制尚未明确. 目的探讨补充外源性锌预处理对心肌保护的作用及其机制. 内容从锌的基本生理作用、预处理心肌保护中的作用及其机制方面进行综述,外源性锌主要是通过激活转录因子NF-E2相关因子2(transcription factor NF-E2-related factor 2,Nrf2)-抗氧化反应元件(antioxidant response element,ARE)抗氧化通路和刺激诱导金属硫蛋白(metallothionein,MT)的产生增加,通过调控线粒体通透性转换孔(mitochondrial permeability transition pore,mPTP)开放及其关闭等机制来减轻MI/RI. 趋向外源性锌主要通过抗氧化这一终末效应达到减轻MI/RI作用,其具体机制尚需进一步的研究探讨.
배경 심기결혈/재관주손상(myocardial ischemia/reperfusion,MI/RI)적발생궤제주요여양화응격손상유관,보충외원성적자대심기진행예처리,능구보호결혈/재관주손상적심기,단구체궤제상미명학. 목적 탐토보충외원성자예처리대심기보호적작용급기궤제. 내용 종자적기본생리작용、예처리심기보호중적작용급기궤제방면진행종술,외원성자주요시통과격활전록인자NF-E2상관인자2(transcription factor NF-E2-related factor 2,Nrf2)-항양화반응원건(antioxidant response element,ARE)항양화통로화자격유도금속류단백(metallothionein,MT)적산생증가,통과조공선립체통투성전환공(mitochondrial permeability transition pore,mPTP)개방급기관폐등궤제래감경MI/RI. 추향 외원성자주요통과항양화저일종말효응체도감경MI/RI작용,기구체궤제상수진일보적연구탐토.
Background The mechanism of myocardial ischemia/reperfusion injury (MI/RI) is mainly due to the oxidative stress injury,and supplying exogenous zinc for myocardial pretreatment can protect myocardium injured by ischemia/reperfusion,but the specific mechanism is still not clear.Objective To investigate the protective effect and its mechanism of supplying exogenous zinc for myocardial pretreatment.Content Summarize the basic physiological role of zinc and the protective effect and mechanism of myocardial pretreatment by supplying exogenous zinc,study whether the exogenous zinc relieves the MI/RI mainly by activating the transcription factor NF-E2-related factor 2 (Nrf2)-antioxidant response element (ARE) antioxidant pathway,stimulating and inducing addition of metallothionein (MT),and also regulating the opening and closing of mitochondrial permeability transition pores (mPTP) and other mechanisms.Trend The exogenous zinc relieves the MI/RI mainly by the terminal effect of antioxidation,however,the specific mechanism requires further research.