摘要
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（transcriptionf actor NF-E2-related factor2，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MFRI。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。
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.
出处
《国际麻醉学与复苏杂志》
CAS
2015年第9期853-857,共5页
International Journal of Anesthesiology and Resuscitation
基金
贵州省科技厅攻关项目（黔科合SY字[2011]3015）
