Exogenous taurine attenuates mitochondrial oxidative stress and endoplasmic reticulum stress in rat cardiomyocytes  

作　　者：Yujie Yang Yue Zhang Xiaoyu Liu Ji Zuo Keqiang Wang Junbo Ge 

机构地区：[1]Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China [2]Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai 200032, China

出　　处：《Acta Biochimica et Biophysica Sinica》2013年第5期359-367,共9页生物化学与生物物理学报（英文版）

摘　　要：Taurine, a conditionally essential amino acid, plays a critical role in cardiovascular function. Here we examined the effect of taurine on mitochondria and endoplasmic reticulum in rat cardiomyocytes during glucose deprivation （GD）. Data showed that cell viabifity, intracellular taurine contents, and taurine transporter expression were decreased during GD. In contrast, an increase in reactive oxygen species and intracellular Ca2＋ contents was observed. GD also caused disrupted mitochondriai membrane potential, apoptotic cell death, and dissociation of unfolded protein response （UPR）- relative proteins in cardiomyocytes. Signal transduction analysis showed that Bcl-2 family protein balance was disturbed, caspase-12 was activated and UPR-relative protein levels were up-regulated. Moreover, pre-treatment with 80 mM exogenous taurine attenuated GD effect in cardio- myocytes. Our results suggest that taurine have beneficial effects on inhibiting mitochondria-dependent cell apoptosis and UPR-associated cell apoptosis and might have clinical implications on acute myocardial infarction in future.Taurine, a conditionally essential amino acid, plays a critical role in cardiovascular function. Here we examined the effect of taurine on mitochondria and endoplasmic reticulum in rat cardiomyocytes during glucose deprivation （GD）. Data showed that cell viabifity, intracellular taurine contents, and taurine transporter expression were decreased during GD. In contrast, an increase in reactive oxygen species and intracellular Ca2＋ contents was observed. GD also caused disrupted mitochondriai membrane potential, apoptotic cell death, and dissociation of unfolded protein response （UPR）- relative proteins in cardiomyocytes. Signal transduction analysis showed that Bcl-2 family protein balance was disturbed, caspase-12 was activated and UPR-relative protein levels were up-regulated. Moreover, pre-treatment with 80 mM exogenous taurine attenuated GD effect in cardio- myocytes. Our results suggest that taurine have beneficial effects on inhibiting mitochondria-dependent cell apoptosis and UPR-associated cell apoptosis and might have clinical implications on acute myocardial infarction in future.

关 键 词：TAURINE taurine transporter glucosedeprivation mitochondrial oxidative stress endoplasmicreticulum stress 

分 类 号：Q949.329[生物学—植物学] Q463