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Drug: Melatonin

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Total 139 results found since Jan 2013.

Melatonin against acute ischaemic stroke dependently via suppressing both inflammatory and oxidative stress downstream signallings.
In conclusion, TLR inflammatory and oxidative stress signallings played crucial roles for brain damage and impaired neurological function after IS that were significantly reversed by Mel therapy. PMID: 32729676 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - July 29, 2020 Category: Molecular Biology Authors: Chen KH, Lin KC, Ko SF, Chiang JY, Guo J, Yip HK Tags: J Cell Mol Med Source Type: research

Inflammatory Cytokines are in Action: Brain Plasticity and Recovery after Brain Ischemia Due to Delayed Melatonin Administration
Brain ischemia is a critical condition which starts because of a decrease in blood circulation to brain. This insufficient blood flow leads to inability to do metabolic functions and to the death of brain tissue. In the acute phase of the stroke, inflammation occurs in the ischemic hemisphere due to the infiltration of blood immune cells from damaged blood-brain barrier (BBB). Infiltrating immune cells because the secretion of various inflammatory mediators, and a secondary damage occurs in the place of stroke.
Source: Journal of Stroke and Cerebrovascular Diseases - September 18, 2021 Category: Neurology Authors: Ulkan Kilic, Birsen Elibol, Merve Beker, Burcugul Altug-Tasa, Ahmet Burak Caglayan, Mustafa Caglar Beker, Bayram Yilmaz, Ertugrul Kilic Source Type: research

Stem cell survival after transplantation impacted by melatonin pre-treatment
When melatonin, a hormone secreted by the pineal gland, was used as a pre-treatment for mesenchymal stem cells (MSCs) prior to their transplantation into the brains of laboratory animals to repair damage from stroke, researchers in China found that the stem cells survived longer after transplantation. Previous studies had shown that 80 percent of transplanted MSCs died within 72 hours of transplantation. By contrast, the melatonin pre-treatment "greatly increased" cell survival, said the researchers...
Source: Health News from Medical News Today - July 24, 2013 Category: Consumer Health News Tags: Stroke Source Type: news

Pre ‐ischemia melatonin treatment alleviated acute neuronal injury after ischemic stroke by inhibiting ER stress‐dependent autophagy via PERK and IRE1 signalings
This article is protected by copyright. All rights reserved.
Source: Journal of Pineal Research - February 7, 2017 Category: Research Authors: Dayun Feng, Bao Wang, Lei Wang, Neeta Abraham, Kai Tao, Lu Huang, Wei Shi, Yushu Dong, Yan Qu Tags: Original Article Source Type: research

Melatonin provides protection against heat stroke ‐induced myocardial injury in male rats
ConclusionsMelatonin may protect against HS‐induced myocardial injury in male rats by mitigating oxidative stress and inflammation.
Source: Journal of Pharmacy and Pharmacology - February 27, 2018 Category: Drugs & Pharmacology Authors: Xiaojing Lin, Tingbao Zhao, Cheng ‐Hsien Lin, Dan Zuo, Zhujun Ye, Shide Lin, Shaonan Wen, Lin Liu, Mao‐Tsun Lin, Ching‐Ping Chang, Chien‐Ming Chao Tags: Research Paper Source Type: research

Circadian rhythms of melatonin, cortisol, and clock gene expression in the hyperacute phase of wake-up stroke: study design and measurement.
PMID: 32991368 [PubMed - as supplied by publisher]
Source: Chinese Medical Journal - September 23, 2020 Category: General Medicine Authors: Zhang XX, Cai XY, Zhao HR, Wang H, Wang DP, Zhang QQ, Wang H, Fang Q Tags: Chin Med J (Engl) Source Type: research

Cryptotanshinone Attenuates Oxygen-Glucose Deprivation/ Recovery-Induced Injury in an in vitro Model of Neurovascular Unit
Conclusions Despite the above limitations, we indicate that the protective mechanism of CTs against OGD/R damage might exert via inhibiting neuron apoptosis and attenuating BBB disruption. Furthermore, we also clarified that CTs inhibited neuronal apoptosis possibly by blocking the activation of MAPK signaling pathways, and CTs alleviating BBB disruption may associated with the regulation of TJPs and MMP-9 in our experiment. Accordingly, CTs will represent a novel and potent candidate for the treatment of CIRI in the future. Ethics Statement This study was carried out in accordance with the recommendations of China�...
Source: Frontiers in Neurology - April 17, 2019 Category: Neurology Source Type: research

Oversleeping: The Effects and Health Risks of Sleeping Too Much
This article originally appeared on the Amerisleep blog. Rosie Osmun is the Creative Content Manager at Amerisleep, a progressive memory foam mattress brand focused on eco-friendly sleep solutions. Rosie writes more posts on the Amerisleep blog about the science of sleep, eco-friendly living, leading a healthy lifestyle and more. -- This feed and its contents are the property of The Huffington Post, and use is subject to our terms. It may be used for personal consumption, but may not be distributed on a website.
Source: Healthy Living - The Huffington Post - January 29, 2016 Category: Consumer Health News Source Type: news

Melatonin supplementation in the subacute phase after ischemia alleviates postischemic sleep disturbances in rats
ConclusionsMelatonin promptly reversed ischemia-induced sleep disturbances. The neuroprotective effects of melatonin on ischemic injury may be partially associated with its role in sleep modulation.
Source: Brain and Behavior - September 14, 2021 Category: Neurology Authors: Shu ‐Mei Hao, Zhi‐Gang Zhong, Wei‐Min Qu, Zhi‐Li Huang, Feng‐Yan Sun, Mei‐Hong Qiu Tags: ORIGINAL ARTICLE Source Type: research

Role of TREK-1 in Health and Disease, Focus on the Central Nervous System
Conclusion and Perspectives Since their cloning 20 years ago, the physiological importance of TREK-1 channels has continued to grow (Figure 3). Today, TREK-1 channels have been shown to be important and their presence is essential in a number of physiopathological processes. Their involvement in these different processes demonstrate the necessity to design pharmacological modulators, activators or inhibitors, of these channels to correct any TREK-1-related dysfunctions. Despites a number of studies and many molecule screenings, only few putative new drugs were identified. The activators belonging to the ML and BL series ...
Source: Frontiers in Pharmacology - April 10, 2019 Category: Drugs & Pharmacology Source Type: research

Melatonin improves neuroplasticity by upregulating the growth‐associated protein 43 (GAP‐43) and NMDAR‐post‐synaptic density‐95 (PSD95) proteins in cultured neurons exposed to glutamate excitotoxicity and in rats subjected to transient focal cerebral ischemia even during a long‐term recovery period
This article is protected by copyright. All rights reserved.
Source: Journal of Pineal Research - December 18, 2013 Category: Research Authors: Wei‐Sheng Juan, Sheng‐Yang Huang, Che‐Chao Chang, Yu‐Chang Hung, Yu‐Wen Lin, Tsung‐Ying Chen, Ai‐Hua Lee, Ai‐Chiang Lee, Tian‐Shung Wu, E‐Jian Lee Tags: Original Article Source Type: research

Melatonin improves neuroplasticity by upregulating the growth‐associated protein‐43 (GAP‐43) and NMDAR postsynaptic density‐95 (PSD‐95) proteins in cultured neurons exposed to glutamate excitotoxicity and in rats subjected to transient focal cerebral ischemia even during a long‐term recovery period
Abstract Recent evidence shows that the NMDAR postsynaptic density‐95 (PSD‐95), growth‐associated protein‐43 (GAP‐43), and matrix metalloproteinase‐9 (MMP‐9) protein enhance neuroplasticity at the subacute stage of stroke. Here, we evaluated whether melatonin would modulate the PSD‐95, GAP‐43, and MMP‐9 proteins in cultured neurons exposed to glutamate excitotoxicity and in rats subjected to experimental stroke. Adult male Sprague–Dawley rats were treated with melatonin (5 mg/kg) or vehicle at reperfusion onset after transient occlusion of the right middle cerebral artery (tMCAO) for 90 min. Animals...
Source: Journal of Pineal Research - January 13, 2014 Category: Research Authors: Wei‐Sheng Juan, Sheng‐Yang Huang, Che‐Chao Chang, Yu‐Chang Hung, Yu‐Wen Lin, Tsung‐Ying Chen, Ai‐Hua Lee, Ai‐Chiang Lee, Tian‐Shung Wu, E‐Jian Lee Tags: Original Article Source Type: research

Agomelatine protects against permanent cerebral ischaemia via the Nrf2-HO-1 pathway.
In this study, we focused on the effect of agomelatine on permanent cerebral ischaemia in a rat model. Male Wistar rats were randomly divided into the following four groups (n = 6/group): sham operating group, permanent ischaemic model group, permanent ischaemic model plus agomelatine (40 mg/kg, i.p) group and permanent ischaemic model plus melatonin (10 mg/kg, i.p) group. Twenty-four h after ischaemic onset, we investigated the neurological deficits and infarct volume using neurological deficit scores, 2,3,5-triphenyltetrazolium chloride (TTC) and transmission electron microscopy (Kochanski et al.). Moreover, we a...
Source: European Journal of Pharmacology - February 17, 2020 Category: Drugs & Pharmacology Authors: Chumboatong W, Khamchai S, Tocharus C, Govitrapong P, Tocharus J Tags: Eur J Pharmacol Source Type: research

Article A potent antioxidant endogenous neurohormone melatonin, rescued MCAO by attenuating oxidative stress-associated neuroinflammation
IIschemic stroke is an acute neurological syndrome either due to permanent or temporary obstruction of blood. Such obstruction immediately triggers abrupt pathological cascading processes, which collectively lead to neuronal cell death. Oxidative stress and neuroinflammation in ischemic stroke are critical regulating events that ultimately lead to neuronal death. Complicated interplay exists between the two processes which occur through several stages. Most often, oxidative stress precedes the inflammatory mechanisms and includes several interconnected cascades that underlie the ischemic stroke pathology. In continuation o...
Source: Frontiers in Pharmacology - August 20, 2020 Category: Drugs & Pharmacology Source Type: research

A Potent Antioxidant Endogenous Neurohormone Melatonin, Rescued MCAO by Attenuating Oxidative Stress-Associated Neuroinflammation
Ischemic stroke is an acute neurological syndrome either due to permanent or temporary obstruction of blood. Such obstruction immediately triggers abrupt pathological cascading processes, which collectively lead to neuronal cell death. Oxidative stress and neuroinflammation in ischemic stroke are critical regulating events that ultimately lead to neuronal death. Complicated interplay exists between the two processes which occur through several stages. Most often, oxidative stress precedes the inflammatory mechanisms and includes several interconnected cascades that underlie the ischemic stroke pathology. In continuation of...
Source: Frontiers in Pharmacology - August 20, 2020 Category: Drugs & Pharmacology Source Type: research