Intravenous administration of melatonin reduces the intracerebral cellular inflammatory response following transient focal cerebral ischemia in rats. - Wikidata - wikimedia - TriplyDB

Intravenous administration of melatonin reduces the intracerebral cellular inflammatory response following transient focal cerebral ischemia in rats.

Intravenous administration of melatonin reduces the intracerebral cellular inflammatory response following transient focal cerebral ischemia in rats.

http://www.wikidata.org/entity/Q48248885

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Neuroprotection and antioxidants Peptidylarginine Deiminases as Drug Targets in Neonatal Hypoxic-Ischemic Encephalopathy Blood-brain barrier integrity and glial support: mechanisms that can be targeted for novel therapeutic approaches in stroke Neuroprotective effect of melatonin: a novel therapy against perinatal hypoxia-ischemia Radiation protection following nuclear power accidents: a survey of putative mechanisms involved in the radioprotective actions of taurine during and after radiation exposure Melatonin promotes oligodendroglial maturation of injured white matter in neonatal rats.Protective effect of melatonin upon neuropathology, striatal function, and memory ability after intracerebral hemorrhage in rats.Hypoxic ischemic brain injury: Potential therapeutic interventions for the future.Melatonin attenuates intermittent hypoxia-induced lipid peroxidation and local inflammation in rat adrenal medulla.Melatonin Counteracts at a Transcriptional Level the Inflammatory and Apoptotic Response Secondary to Ischemic Brain Injury Induced by Middle Cerebral Artery Blockade in Aging Rats Propofol Suppressed Hypoxia/Reoxygenation-Induced Apoptosis in HBVSMC by Regulation of the Expression of Bcl-2, Bax, Caspase3, Kir6.1, and p-JNK Melatonin: buffering the immune system Melatonin-based therapeutics for neuroprotection in stroke.Effects of melatonin on cognitive impairment and hippocampal neuronal damage in a rat model of chronic cerebral hypoperfusion The Effect of Circadian Melatonin Levels on Inflammation and Neurocognitive Functions Following Coronary Bypass Surgery Effects of melatonin in experimental stroke models in acute, sub-acute, and chronic stages Partial neural protection with prophylactic low-dose melatonin after asphyxia in preterm fetal sheep.Oxidative stress and its role in the pathogenesis of ischaemic stroke.Molecular chaperones and hypoxic-ischemic encephalopathy Neuroimmunomodulation in unipolar depression: a focus on chronobiology and chronotherapeutics.The role of neuroendocrine pathways in prognosis after stroke.Melatonin as an Antioxidant for Stroke Neuroprotection.Inflammation and the Silent Sequelae of Stroke.Treatment of acute cerebral ischemia using animal models: a meta-analysis.Melatonin inhibits matrix metalloproteinase-9 (MMP-9) activation in the lipopolysaccharide (LPS)-stimulated RAW 264.7 and BV2 cells and a mouse model of meningitis.Inhibitory effects of melatonin on the lipopolysaccharide-induced CC chemokine expression in BV2 murine microglial cells are mediated by suppression of Akt-induced NF-κB and STAT/GAS activity.Melatonin protects against transient focal cerebral ischemia in both reproductively active and estrogen-deficient female rats: the impact of circulating estrogen on its hormetic dose-response.Melatonin: Pharmacology, Functions and Therapeutic Benefits.Dual effects of melatonin on oxidative stress after surgical brain injury in rats.Melatonin and Nitrones As Potential Therapeutic Agents for Stroke.Melatonin treatment reduces astrogliosis and apoptosis in rats with traumatic brain injury.Neuroprotective effect of melatonin against hypoxia-induced retinal ganglion cell death in neonatal rats.Melatonin augments hypothermic neuroprotection in a perinatal asphyxia model.Melatonin ameliorates hippocampal nitric oxide production and large conductance calcium-activated potassium channel activity in chronic intermittent hypoxia.Utility of melatonin to treat surgical stress after major vascular surgery--a safety study.Early reperfusion improves the recovery of contralateral electrophysiological diaschisis following focal cerebral ischemia in rats.The effects of long-term exposure of magnetic field via 900-MHz GSM radiation on some biochemical parameters and brain histology in rats.Optimal Percoll concentration facilitates flow cytometric analysis for annexin V/propidium iodine-stained ischemic brain tissues.Melatonin alleviates secondary brain damage and neurobehavioral dysfunction after experimental subarachnoid hemorrhage: possible involvement of TLR4-mediated inflammatory pathway.The neuroprotective role of melatonin in neurological disorders.

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Intravenous administration of melatonin reduces the intracerebral cellular inflammatory response following transient focal cerebral ischemia in rats.

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Journal of Pineal Research

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Chien-Chih Huang

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E-Jian Lee

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Hung-Yi Chen

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I-Ping Yang

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Ming-Yang Lee

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Shur-Tzu Chen

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Tian-Shung Wu

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Tsung-Ying Chen

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Yun-Shang Hsu

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P2860

Tissue-plasminogen activator-induced ischemic brain injury is reversed by melatonin: role of iNOS and Akt.

Melatonin decreases neurovascular oxidative/nitrosative damage and protects against early increases in the blood-brain barrier permeability after transient focal cerebral ischemia in mice.

Inflammatory mediators and stroke: new opportunities for novel therapeutics.

Excitotoxicity, oxidative stress, and the neuroprotective potential of melatonin.

Chemical and physical properties and potential mechanisms: melatonin as a broad spectrum antioxidant and free radical scavenger.

Biochemical reactivity of melatonin with reactive oxygen and nitrogen species: a review of the evidence.

The utility of melatonin in reducing cerebral damage resulting from ischemia and reperfusion.

mGluRI targets microglial activation and selectively prevents neuronal cell engulfment through Akt and caspase dependent pathways

Activation of microglial poly(ADP-ribose)-polymerase-1 by cholesterol breakdown products during neuroinflammation: a link between demyelination and neuronal damage.

Neuroprotective effect of exogenous microglia in global brain ischemia.

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cerebral infarction