Melatonin and Ischemic Stroke: Mechanistic Roles and Action

Andrabi, Syed Suhail; Parvez, Suhel; Tabassum, Heena

doi:10.1155/2015/384750

Cited by 54 publications

(56 citation statements)

References 130 publications

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“…In the opinion of Escribano and co-worker [38], decrease of melatonin level in this pathology is a part of its pathogenic features. Thus, in cerebral ischemia melatonin reveals antioxidant, antiapoptotic and anti-inflammatory properties [39]. In ischemic stroke patients the impaired nocturnal melatonin excretion is associated with altered sleep-wake rhythm, increased blood cortisol level and decrease of T lymphocytes number [40].…”

Section: Brain Ischemiamentioning

confidence: 99%

Age-Related Changes in the Melatonin and Thymulin Biorhythms as Risk Factors for Human Neurodegenerative Diseases

Labunets¹

2017

GGS

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MelatoninNumerous studies suggest that melatonin is the main regulator of circadian and circannual rhythms both in mammals and humans CRIMSONpublishers http://www.crimsonpublishers.com Irina F Labunets* AbstractThe frequency of age-related neurodegenerative pathology, such as Parkinson's and Alzheimer's diseases, brain ischemia and multiple sclerosis increases worldwide and has great socio-economic implications. The use of approaches based on investigation the pathogenic factors of their development may be perspective in the prevention and treatment of such diseases.Circadian and circannual rhythms play a key role in the adaptative changes of human neuroendocrine and immune systems to the light and temperature. The rhythmicity of these systems is disturbed in human aging that may be connected with desynchronosis of pineal gland melatonin production. This process becomes more intensive during development of the neurodegenerative diseases.Thymic endocrine function (thymulin production) is the important part of chronobiological organization of immune system. The circadian and circannual rhythms of thymulin depend on the synchronizing influence of melatonin. Melatonin production disorders lead to the intra-immune desynchronosis via disturbances of the circadian and circannual rhythms of thymulin and its interactions with the endocrine glands (hypophysis, adrenal glands, gonads etc) both in aging and age pathology.Melatonin treatment improves sleep-wake rhythm and produces antiapoptotic, antioxidant and anti-inflammatory effects in the brain at neurodegenerative diseases and slows down development of this pathology. Moreover, melatonin treatment leads to the suppression of age-related changes in the rhythmicity of immune and neuroendocrine systems functions. Such melatonin effect is realized via synchronous influence on the circadian and circannual rhythms of thymulin production.Therefore melatonin seems to be perspective for restoring disturbed rhythmicity of immune and neuroendocrine systems in:A. accelerated human aging with pineal gland dysfunction and B. Patients of different age and sex suffering from neurodegenerative diseases making individual hormone dose correction.

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Section: Brain Ischemiamentioning

confidence: 99%

Age-Related Changes in the Melatonin and Thymulin Biorhythms as Risk Factors for Human Neurodegenerative Diseases

Labunets¹

2017

GGS

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“…High levels of melatonin compared to other cellular compartments have been identified in mitochondria [24,25,26,27,28]. A variety of in vitro and in vivo studies have proven that melatonin targets mitochondria to reduce oxidative stress [29,30,31,32,33,34,35,36]. This results in decreased apoptosis, improved metabolic status, and an elevated survival rate of cultured cells, unicellular organisms, animals, and plants, which suffer with oxidative stress [37,38,39,40,41,42,43,44,45].…”

Section: Introductionmentioning

confidence: 99%

Melatonin: A Mitochondrial Targeting Molecule Involving Mitochondrial Protection and Dynamics

Tan

Manchester

Qin

et al. 2016

IJMS

312

256

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Melatonin has been speculated to be mainly synthesized by mitochondria. This speculation is supported by the recent discovery that aralkylamine N-acetyltransferase/serotonin N-acetyltransferase (AANAT/SNAT) is localized in mitochondria of oocytes and the isolated mitochondria generate melatonin. We have also speculated that melatonin is a mitochondria-targeted antioxidant. It accumulates in mitochondria with high concentration against a concentration gradient. This is probably achieved by an active transportation via mitochondrial melatonin transporter(s). Melatonin protects mitochondria by scavenging reactive oxygen species (ROS), inhibiting the mitochondrial permeability transition pore (MPTP), and activating uncoupling proteins (UCPs). Thus, melatonin maintains the optimal mitochondrial membrane potential and preserves mitochondrial functions. In addition, mitochondrial biogenesis and dynamics is also regulated by melatonin. In most cases, melatonin reduces mitochondrial fission and elevates their fusion. Mitochondrial dynamics exhibit an oscillatory pattern which matches the melatonin circadian secretory rhythm in pinealeocytes and probably in other cells. Recently, melatonin has been found to promote mitophagy and improve homeostasis of mitochondria.

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“…It has been reported that Mel, a pineal hormone, as well as its metabolites, display important antioxidant properties in the nervous system [13, 14]. Mel has been previously recognized for its protective effects, which include properties related to radical scavenging and antioxidant potential [10].…”

Section: Introductionmentioning

confidence: 99%

Melatonin pre-treatment mitigates SHSY-5Y cells against oxaliplatin induced mitochondrial stress and apoptotic cell death

et al. 2017

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Oxaliplatin (Oxa) treatment to SH-SY5Y human neuroblastoma cells has been shown by previous studies to induce oxidative stress, which in turn modulates intracellular signaling cascades resulting in cell death. While this phenomenon of Oxa-induced neurotoxicity is known, the underlying mechanisms involved in this cell death cascade must be clarified. Moreover, there is still little known regarding the roles of neuronal mitochondria and cytosolic compartments in mediating Oxa-induced neurotoxicity. With a better grasp of the mechanisms driving neurotoxicity in Oxa-treated SH-SY5Y cells, we can then identify certain pathways to target in protecting against neurotoxic cell damage. Therefore, the purpose of this study was to determine whether one such agent, melatonin (Mel), could confer protection against Oxa-induced neurotoxicity in SH-SY5Y cells. Results from the present study found Oxa to significantly reduce SH-SY5Y cell viability in a dose-dependent manner. Alternatively, we found Mel pre-treatment to SH-SY5Y cells to attenuate Oxa-induced toxicity, resulting in a markedly increased cell viability. Mel exerted its protective effects by regulating reactive oxygen species (ROS) production and reducing superoxide radicals inside Oxa-exposed. In addition, we observed pre-treatment with Mel to rescue Oxa-treated cells by protecting mitochondria. As Oxa-treatment alone decreases mitochondrial membrane potential (Δψm), resulting in an altered Bcl-2/Bax ratio and release of sequestered cytochrome c, so Mel was shown to inhibit these pathways. Mel was also found to inhibit proteolytic activation of caspase 3, inactivation of Poly (ADP Ribose) polymerase, and DNA damage, thereby allowing SH-SY5Y cells to resist apoptotic cell death. Collectively, our results suggest a role for melatonin in reducing Oxa induced neurotoxicity. Further studies exploring melatonin’s protective effects may prove successful in eliciting pathways to further alter the neurotoxic pathways of platinum compounds in cancer treatment.

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Melatonin and Ischemic Stroke: Mechanistic Roles and Action

Cited by 54 publications

References 130 publications

Age-Related Changes in the Melatonin and Thymulin Biorhythms as Risk Factors for Human Neurodegenerative Diseases

Age-Related Changes in the Melatonin and Thymulin Biorhythms as Risk Factors for Human Neurodegenerative Diseases

Melatonin: A Mitochondrial Targeting Molecule Involving Mitochondrial Protection and Dynamics

Melatonin pre-treatment mitigates SHSY-5Y cells against oxaliplatin induced mitochondrial stress and apoptotic cell death

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