Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.
Cardioprotective effect of melatonin against ischaemia/reperfusion damage
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Melatonin (N-acetyl-5-methoxytryptamine) has been shown by several workers to protect the heart against ischaemia/reperfusion damage. Melatonin, both in the picomolar and micromolar range, significantly reduces infarct size and improves functional recovery during reperfusion. This may be due to its free radical scavenging and anti-oxidant effects, while the melatonin receptor and its marked anti-adrenergic actions may also be involved. The latter is mediated by nitric oxide (NO), guanylyl cyclase and protein kinase C (PKC). Melatonin-induced cardioprotection is associated with activation of protein kinase B (PKB), extracellular signal-regulated kinase (ERK1/2) (the Reperfusion Injury Salvage Kinase (RISK) pathway) and signal activator and transducer 3 (STAT-3) (the Survivor Activating Factor Enhancement (SAFE) pathway) during reperfusion and inhibition of the mitochondrial permeability transition pore (MPTP). Very little is known about the effect of melatonin on myocardial substrate metabolism. Melatonin was demonstrated to be involved in the regulation of whole body glucose homeostasis via its effects on pancreatic insulin secretion and may thus indirectly affect myocardial substrate metabolism in a circadian manner.