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Melatonin regulates neuroinflammation ischemic stroke damage through interactions with microglia in reperfusion phase.
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Even today, ischemic stroke is a major cause of death and disabilities because of its high incidence, limited treatments and poor understanding of the pathophysiology of ischemia/reperfusion, neuroinflammation and secondary injuries following ischemic stroke. The function of microglia as a part of
[Melatonin in the correction of sleep in post-stroke patients].
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OBJECTIVE
To assess an effect of melatonin on quality of life and effectiveness of rehabilitation in patients with ischemic stroke (IS) suffered from insomnia due to sleep initiation disturbance.
METHODS
Sixty post-stroke patients with insomnia were stratified into two groups matched for
Nocturnal urine melatonin and 6-sulphatoxymelatonin excretion at the acute stage of ischaemic stroke.
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Melatonin's neuroprotective action has been demonstrated in experimental models of brain ischaemia. The relationship between stroke and melatonin levels has been based on scarce and small sample size studies. In addition, the changes have not been correlated with the age of patients. We compared
Beneficial effects of melatonin on stroke-induced muscle atrophy in focal cerebral ischemic rats.
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MUSCLE ATROPHY IS THE RESULT OF TWO OPPOSING CONDITIONS THAT CAN BE FOUND IN PATHOLOGICAL OR DISEASED MUSCLES: an imbalance in protein synthesis and degradation mechanisms. Thus, we investigated whether exogenous melatonin could regulate muscle components in stroke-induced muscle atrophy in rats.
Impaired nocturnal melatonin in acute phase of ischaemic stroke: cross-sectional matched case-control analysis.
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Quantitative data on melatonin in stroke patients are scarce. A gender- and age-matched cross-sectional case-control study in 33 patients with ischaemic stroke was performed and associations between nocturnal melatonin and other factors (e.g. cortisol) were evaluated. Clinical and laboratory (e.g.
Dynamics of oxidative stress and urinary excretion of melatonin and its metabolites during acute ischemic stroke.
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Oxidative stress is a leading cause of neuronal damage in ischemic stroke. Melatonin may play a role in the antioxidant response. Melatonin and its metabolites may be involved in the modulation of oxidative stress in human acute stroke. No data are available in humans to establish this relationship.
Melatonin-secreting pineal gland: a novel tissue source for neural transplantation therapy in stroke.
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Chronic systemic melatonin treatment attenuates abnormalities produced by occlusion of middle cerebral artery (MCA) in adult rats. Because the pineal gland secretes high levels of melatonin, we examined in the present study whether transplantation of pineal gland exerted similar protective effects
Melatonin receptor agonists for treating delirium in elderly patients with acute stroke.
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BACKGROUND
Delirium is considered to worsen life prognosis in elderly patients with stroke. We examined the effects of the melatonin receptor agonist ramelteon for treating delirium in elderly stroke patients with insomnia in comparison to the other drugs.
METHODS
Elderly patients with delirium and
When melatonin gets on your nerves: its beneficial actions in experimental models of stroke.
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This article summarizes the evidence that endogenously produced and exogenously administered melatonin reduces the degree of tissue damage and limits the biobehavioral deficits associated with experimental models of ischemia/reperfusion injury in the brain (i.e., stroke). Melatonin's efficacy in
[Influence of pineal hormone melatonin on behavioral disturbances and neurological status of animals after hemorrhagic stroke].
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Experimental hemorrhagic stroke causes behavior and locomotor activity with memory impairment and neurological disturbances in rats. These shifts are weaker in the evening hours than after morning testing. The repeated administration of the pineal gland hormone melatonin (melaxen) during one week
Melatonin reduces infarction volume in a photothrombotic stroke model in the wild-type but not cyclooxygenase-1-gene knockout mice.
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Cyclooxygenase (COX)-2 plays a harmful role in cerebral ischemic/reperfusion injury, but the role of COX-1 is uncertain. In the present study, cerebral infarct was induced by photothrombosis. Intraperitoneal injections of melatonin at 15 g/kg or its vehicle were made at 0.5 hr before stroke and 24
Melatonin reduces nitric oxide level during ischemia but not blood-brain barrier breakdown during reperfusion in a rat middle cerebral artery occlusion stroke model.
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Melatonin is a potent antioxidant and free radical scavenger. Previously, we showed that a single injection of melatonin before ischemia significantly reduced the infarct volume in both permanent and 3-hr middle cerebral artery occlusion (MCAO) rat stroke models. Nitric oxide (NO) and other free
Physiological and pharmacological roles of melatonin in the pathophysiological components of cellular injury after ischemic stroke
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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
Melatonin and Ischemic Stroke: Mechanistic Roles and Action.
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Stroke is one of the most devastating neurological disabilities and brain's vulnerability towards it proves to be fatal and socio-economic loss of millions of people worldwide. Ischemic stroke remains at the center stage of it, because of its prevalence amongst the several other types attacking the
Enhanced protection by melatonin and meloxicam combination in a middle cerebral artery occlusion model of acute ischemic stroke in rat.
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Mixed efficacy of neuroprotective drugs in clinical trials has led to the emergence of the approach of combination therapy in stroke. The present study was carried out to investigate the effect of the combination of melatonin (potent antioxidant) and meloxicam (preferential inhibitor of
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