In vitro and in vivo study on prevention of myocardial ischemic injury by taurine

Myocardial ischemia (MI) often causes angina, arrhythmia, and cardiac insufficiency, sometimes resulting in death. Ischemia-induced myocardial tissue damage is attributed to the hypoxic damage of myocardial cells producing apoptosis and decreased proliferation. Taurine has been shown to improve MI, but its mechanism is largely unknown.

We demonstrated that TauT is critical for the attenuation of myocardial ischemic damage by taurine, facilitating taurine absorption and synthesis. These findings provided new insights and a theoretical foundation for future studies examining taurine as a potential treatment for MI.

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). 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. We evaluated the indicators of MI and damage, including lactic dehydrogenase (LDH), creatine kinase (CK), and cardiac troponin I (cTnI). 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).

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. Pretreatment with taurine alleviated the ischemic damage, with concomitant elevation of intracellular taurine concentrations. Molecular mechanism analysis showed that pretreatment with taurine upregulated the TauT, CDO, and CSD, 2 rate-limiting enzymes involved in taurine synthesis. These effects facilitated both taurine transport into cells and taurine synthesis, leading to taurine accumulation. 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. Conclusions: We demonstrated that TauT is critical for the attenuation of myocardial ischemic damage by taurine, facilitating taurine absorption and synthesis. These findings provided new insights and a theoretical foundation for future studies examining taurine as a potential treatment for MI.