MAPK activation and apoptotic alterations in hearts subjected to calcium paradox are attenuated by taurine.

摘要: Objective: The Ca2+-paradox is an important phenomenon to study cell injury induced by Ca2+-overload in myocardium. Although intracellular acts as a trigger and modulator of death due apoptosis under various pathophysiological conditions, the presence hearts subjected has not been demonstrated. Since taurine attenuates changes cardiac function Ca2+-paradox, this investigated occurrence mechanisms Ca2+-paradoxic treated absence taurine. Methods: was perfusing isolated rat heart with Ca2+-free medium for 5 min followed reperfusion Ca2+-containing 30 min. Apoptosis related signal transduction were determined perfused or without 10 mM taurine. Results: Marked alterations seen reperfused Unlike total protein contents phosphorylated p38 mitogen-activated kinase (MAPK), extracellular regulated (ERK)1, ERK2 c-jun amino-terminal increased 125±8.6%, 296±14.3%, 213±8.5% 133±4.2%, respectively vs. control. Caspase-3 Bcl-2 also 193±10.2% 134±5.0% control whereas Bad ratio Bcl-2/Bad depressed 32±10.8% 0.23±0.5% hearts. 30 min evident at 10 min Ca2+-repletion but similar 60 min Ca2+-repletion. These apoptotic pathway cardiomyocytes prevented taurine. Furthermore, attenuated KCl- ATP-induced increase concentration Ca2+ cardiomyocytes. Conclusions: This suggests that dysfunction may be associated apoptosis. In addition, beneficial effects on attenuation MAPK