| BackgroundInducing arrhythmias and even heart failure, acute myocardial ischemia (AMI) is one of the most serious cardiovascular events and the most common cause of mortality worldwide. Although percutaneous coronary intervention (PCI) has been one of the usual therapeutic interventions for coronary heart disease, ischemia reperfusion injury will still lead to the myocardial damage. So supplementation of myocardial preservation drug along with percutaneous coronary intervention will have the effect of icing on the cake. Taurine, a β-aminosulfonic acid, is the most abundant free amino acid in excitable mammalian tissues, with intracellular concentrations of20-70mmol/kg in the heart. Accumulating evidence indicates that taurine may play a cytoprotective role in the heart. Indeed, the oral supplementation of taurine has been shown to be effective in animal models and human patients with congestive heart failure and cardiomyopathy. The main mechanisms behind the cytoprotective effects of taurine include the maintenance of calcium (Ca2+), homeostasis, the regulation of osmotic balance and antioxidant and anti-apoptotic activity. Maintenance of the large intracellular taurine pool mainly depends upon the activity of taurine transporter (TAUT). Coronary artery bypass grafting and the spontaneously hypertension have been demonstrated to decrease the the taurine content in the myocardium with unknow mechanism. Whether the taurine content in the myocardium will be changed in acute myocardial ischemia, and whether the supplementation of exogenous taurine will be protective in myocardium, will be explored in this study. And the specific mechanism will also be detected.MethodsThe cultured cardiocytes which were exposed to glucose deprivation(GD) injury and hypoxia and the acute myocardial ischemic rats with or without taurine treatment were investigated. The morphology of cardiac tissues, the apoptosis of cardiocytes and the heart function were detected. Taurine contents were measured by HPLC. The mRNA and protein expressions of TAUT and TonEBP were measured by RT-PCR and western-blot respectively.ResultsTaurine treatment could reverse the apoptosis induced by GD injury, hypoxia and acute myocardial ischemia and effectively protect the myocardium. Our data showed that taurine contents and TAUT expression levels were significantly decreased when cultured cardiocytes and cardiac tissues subjected to GD injury, hypoxic or ischemic stress. Moreover, taurine treatment (lOOmg/kg/d) clearly up-regulated the TAUT expressions and elevated the taurine contents in ischemic myocardial tissues. In vitro, Low dose (40mM or80mM) but not high dose (120mM) of taurine significantly induced the TAUT expressions and elevated the intracellular taurine contents in GD injury and hypoxic cardiocytes. TAUT expressions were in accordance with the TonEBP expressions.ConclusionsTaurine provided the protective effects on ischemic myocardium. Low^dose but not high dose of taurine up-regulated the TAUT expressions through up-regulated the TonEBP expressions and the increased the intra-cardiocyte taurine contents in GD injury, hypoxia and acute myocardial ischemia.The potential application of this workThe downregulation of TAUT expression and decreased concentrations of taurine occurred30min after modeling, which indicates that the concentration of taurine may be an early diagnosis marker for AMI. The mechanism of myocardial protective effect of taurine was explained to provide the theoretical and experimental evidence for the clinical application of taurine in acute myocardial infarction patients.Originalities of this workIt is the first time to reveal that different concentrations of taurine have the different function of regulation of TAUT expressions. It is the first time to reveal that concentration of taurine in myocardium may be an early diagnosis marker for acute myocardial infarction patients.
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