牛磺酸保护心肌缺血-再灌注损伤的研究进展  

Progress of protective effect of taurine on cardiac ischemia-reperfusion injury

作　　者：李开济[1] 贺宝玲[1] 田增有[1] 侯阳阳[1] 张艳敏[1] 门秀丽[1] 吴静[1] 

机构地区：[1]河北联合大学基础医学院,河北唐山063000

出　　处：《现代预防医学》2014年第21期3967-3969,共3页Modern Preventive Medicine

基　　金：国家自然科学基金(81370477;81370918);河北省卫生厅医学研究重点课题(20130060)

摘　　要：缺血-再灌注损伤(Ischemia-Reperfusion Injury,IRI)主要由细胞内高渗肿胀、Ca2+超载和氧化应激引起。牛磺酸是体内一种含量丰富的β-氨基酸,可从多个方面保护心肌细胞。作为渗透因子,牛磺酸的外流有利于细胞内的渗透压下降,维持细胞容量。丝裂原活化蛋白激酶(Mitogen Activated Protein Kinase,MAPK)家族的多个信号通路参与Ca2+超载诱导的心肌细胞凋亡,补充牛磺酸可抑制上述凋亡信号。牛磺酸通过修饰线粒体tRNA可促进线粒体编码蛋白质的合成,改善线粒体功能和细胞能量代谢,减少自由基形成,保护缺血-再灌注心肌。总之,牛磺酸对缺血-再灌注心肌的保护具有重要的临床意义,但剂量和时间需要精细调控。Ischemia-reperfusion injury （IRI） is mainly induced by intracellular hyper-osmoticity and cell swelling, Ca2＋ overload and oxidative stress. Taurine is an abundant 13 -amino acid that regulates several events to protect the cardiomyocytes from injury. As an osmolyte, the extrusion of taurine helps to decrease the intracellular osmotic pressure, and normalize cell volume. There are multiple signaling pathways of mitogen-activated protein kinase （MAPK） family involved in Ca2＋ overload-induced cardiomyocytes apoptosis. Supplementation of taurine can inhibit these apoptotic signals. The antioxidant effect of taurine is mainly through its modification on mitochondrial tRNA, which promotes synthesis of mitochondrial encoded proteins, then improves mitochondrial function and cellular energy metabolism, prevents mitochondrial oxidant production. These protective effects of taurine on ischemia-reperfusion heart have important clinical significance, though the dose and duration need to be carefully grasped.

关 键 词：牛磺酸 缺血-再灌注损伤 钙超载 活性氧 

分 类 号：R113[医药卫生—公共卫生与预防医学]