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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, RESULTS. Meshes: Animals, Apoptosis, Creatine, Myocytes, Cardiac, Phosphorylation, Protein Kinases, Proto-Oncogene Proteins c-akt, Rats, Ribose, Signal Transduction.
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Does supplementation of creatine and ribose prevent apoptosis in ischemic cardiomyocytes? Context: To alleviate ischemia-induced injury in the myocardium, a tissue that depends critically on energy-yielding processes, creatine may be used to enhance energy metabolism, whereas D-ribose may provide building blocks for ATP synthesis. We test the hypothesis that simultaneous supplementation of creatine+D-ribose protects non-irreversibly injured ischemic cardiomyocytes by reducing apoptosis. When H9c2 cardiomyocytes were exposed to 24-h ischemia (1% O(2) with glucose deprivation), viability was severely compromised, but administration of 2.5 mM creatine + 5 mM D-ribose alleviated the fall in viability, whereas 2.5 mM creatine or 5 mM D-ribose did not. These findings correlated with up-regulation of protein kinase B (Akt) phosphorylation. Creatine+D-ribose also blunted adenosine monophosphate-activated protein kinase (AMPK) and down-regulated apoptosis by reducing caspase-3 activation and poly (ADP-ribose) polymerase (PARP) cleavage.
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Simultaneous administration of creatine+D-ribose confers anti-ischemic protection that was absent when treating cardiomyocytes with either creatine or D-ribose. The involved mechanisms stem from the Akt and AMPK signaling pathways. These findings may form the basis of a paradigm whereby re-energization of non-irreversibly damaged cardiomyocytes is a critical step to counteract apoptosis. Final Decision: yes