Abstract
Apart from its metabolic or physiological functions, melatonin has a potent cytoprotective activity in the physiological and pathological conditions. It is synthetized by the pineal gland and released into the blood circulation but particularly cerebrospinal fluid in a circadian manner. It can also easily diffuse through cellular membranes due its small size and lipophilic structure. Its cytoprotective activity has been linked to its potent free radical scavenger activity with the desirable characteristics of a clinically- reliable antioxidant. Melatonin detoxifies oxygen and nitrogen-based free radicals and oxidizing agents, including the highly toxic hydroxyl-and peroxynitrite radicals, initiating cellular damage. However, the cytoprotective activity of melatonin is complex and cannot be solely limited to its free radical scavenger activity. It regulates cellular signaling pathways through receptor– dependent and independent mechanisms. Most of these downstream molecules, such as PI3K/AKT pathway components, also contribute to the cytoprotective effects of melatonin. In this term, melatonin is a promising molecule for the treatment of neurodegenerative disorders, such as ischemic stroke, which melatonin reduces ischemic brain injury in animal models of ischemic stroke. It regulates also circadian rhythm proteins after ischemic stroke, playing roles in cellular survival. In this context, present article summarizes the possible role of melatonin in the pathophysiological events after ischemic stroke.
Highlights
Stroke is one of the leading causes of death and long-term disability worldwide [1] with increasing incidence rates in low and middle-income countries [2]
Patients survived from an ischemic stroke are treated with tissue plasminogen activator that helps to relieve the obstruction in the blood vessels [6]
Our group evaluated the effect of melatonin on the production of nitric oxide and our results demonstrate that melatonin treatment significantly downregulates neuronal NOS (nNOS) and inducible NOS (iNOS) after ischemic brain injury [7,47]
Summary
Stroke is one of the leading causes of death and long-term disability worldwide [1] with increasing incidence rates in low and middle-income countries [2]. The pathophysiologic mechanisms underlying ischemic stroke or ischemia/reperfusion injury in humans include loss of the prooxidant/antioxidant balance, excitotoxicity and related increase in intracellular Ca++ levels, dysfunction in mitochondrial processes, increased neuroinflammation and eventually apoptotic neuronal cell death [8].
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