NDLI: Neuroprotective effect of chrysin on hyperammonemia mediated neuroinflammatory responses and altered expression of astrocytic protein in the hippocampus.

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Neuroprotective effect of chrysin on hyperammonemia mediated neuroinflammatory responses and altered expression of astrocytic protein in the hippocampus.

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Neuroprotective effect of chrysin on hyperammonemia mediated neuroinflammatory responses and altered expression of astrocytic protein in the hippocampus.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Mani, Renuka Natesan, Vijayakumar Arumugam, Ramakrishnan
Description	Country affiliation: India Author Affiliation: Mani R ( Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar 608002, India.); Natesan V ( Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar 608002, India. Electronic address: nvkbiochem@yahoo.co.in.); Arumugam R ( Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar 608002, India.)
Abstract	Neuroinflammation is an innate immune response in the central nervous system (CNS) against metabolic and pathogenic toxic wastes. The main hypothesis implies that a state of hyperammonemia which is accountable for both direct and indirect modification in ammonia metabolism with an elevated production of inflammatory cytokines. This study was constructed to explore the modulating effect of chrysin on rudimentary pathophysiologic mechanisms of ammonium chloride (NH Cl) mediated neuroinflammation in the experimental hyperammonemic rats. NH Cl was injected intraperitonally (i.p) in male albino wistar rats for a time period of thrice a week for eight consecutive weeks. Initially, the levels of brain ammonia and water content were assessed. Immunohistochemical, RT-PCR and western blotting analysis revealed that the expression of glutamine synthetase (GS) activity and glial fibrillar acidic protein (GFAP) were down-regulated, whereas the expression of TNF- , IL-1ß, IL-6, p65 NF-κB, iNOS and COX-2 were up-regulated in brain tissue of hyperammonemic rats. Oral supplementation of chrysin (100mg/kg b.w) to hyperammonemic rats considerably restored the levels of brain ammonia, water content, and the expressions of GS, GFAP, TNF- , IL-1ß, IL-6, p65 NF-κB, iNOS and COX-2. Our findings provided substantial evidence that the chrysin synergistically attenuating the neuroinflammatory mechanism by repressing the expression of proinflammatory cytokines and up-regulating the astrocytic protein expressions via ammonia-reducing strategies. This data suggests that chrysin effectively acts as a therapeutic agent to treat hyperammonemia mediated neuroinflammation.
File Format	HTM / HTML
ISSN	07533322
Volume Number	88
e-ISSN	19506007
Journal	Biomedicine & Pharmacotherapy
Language	English
Publisher	Elsevier
Publisher Date	2017-04-01
Publisher Place	France
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Pharmacology Astrocytes Metabolism Flavonoids Pharmacology Hippocampus Hyperammonemia Drug Therapy Inflammation Nerve Tissue Proteins Biosynthesis Neuroprotective Agents Ammonium Chloride Animals Drug Effects Pathology Brain Chemistry Cytokines Chemically Induced Male Molecular Docking Simulation Rna, Messenger Genetics Rats Rats, Wistar Up-regulation Journal Article
Content Type	Text
Resource Type	Article
Subject	Medicine Pharmacology

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