![]() Because of its sulfo group, taurine cannot be integrated into proteins, so it always exists in a free state. Taurine is present in sites including the brain, heart, liver, kidney, bone, and muscle, where it stabilizes these tissues and protects the cells. ![]() Taurine, the free amino acid most abundant in excitable tissues, has multiple functions, including maintaining cellular calcium homeostasis, preventing calcium overload, promoting cell proliferation and differentiation, stabilizing cell membranes, scavenging free radicals, and protecting cells from lipid peroxidation ( 1). It manifests as angina, arrhythmia, and cardiac insufficiency because of impaired aerobic metabolism in myocardial cells and the resulting limited energy supply. ![]() Myocardial ischemia (MI) is a common life-threating disease with many adverse effects on the heart. Keywords: Taurine myocardial ischemia (MI) taurine transporter (TauT) cysteine dioxygenase (CDO) cysteine sulfinate decarboxylase (CSD) These findings provided new insights and a theoretical foundation for future studies examining taurine as a potential treatment for MI. In addition, apoptosis inhibition by taurine appeared to be mediated by upregulated Bcl-2 and downregulated BAX, as well as inhibition of calcium overload by suppression of calcium binding protein.Ĭonclusions: We demonstrated that TauT is critical for the attenuation of myocardial ischemic damage by taurine, facilitating taurine absorption and synthesis. These effects facilitated both taurine transport into cells and taurine synthesis, leading to taurine accumulation. Molecular mechanism analysis showed that pretreatment with taurine upregulated the TauT, CDO, and CSD, 2 rate-limiting enzymes involved in taurine synthesis. Pretreatment with taurine alleviated the ischemic damage, with concomitant elevation of intracellular taurine concentrations. Results: Exposure of myocardial cells to ischemia led to the decrease of taurine content, the suppression of cell proliferation, and led to calcium ion overload and apoptosis. We also examined the levels of taurine transporter (TauT), cysteine dioxygenase (CDO), and cysteine sulfinate decarboxylase (CSD) proteins involved in transport and synthesis of taurine in the myocardium and those of 2 apoptosis-associated proteins, namely, Bcl-2 associated X protein (BAX) and B-cell lymphoma-2 (Bcl-2). We evaluated the indicators of MI and damage, including lactic dehydrogenase (LDH), creatine kinase (CK), and cardiac troponin I (cTnI). ![]() To elucidate how taurine might suppress ischemic injury, we established an in vitro ischemia model with isolated primary rat cardiomyocytes cultured without serum or glucose and under hypoxia. Methods: In this study, the relationship between taurine and severity of MI in vivo was evaluated by quantifying myocardial infarct areas and metabolic indicators of myocardial damage and measuring taurine levels in cardiac muscle and plasma by high performance liquid chromatography (HPLC). Taurine has been shown to improve MI, but its mechanism is largely unknown. Ischemia-induced myocardial tissue damage is attributed to the hypoxic damage of myocardial cells producing apoptosis and decreased proliferation.
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