Rutin and Selenium Co-administration Reverse 3-Nitropropionic Acid-Induced Neurochemical and Molecular Impairments in a Mouse Model of Huntingtons Disease
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Date
2020
Journal Title
Journal ISSN
Volume Title
Type
Article
Publisher
Springer
Series Info
Neurotoxicity Research
37
37
Scientific Journal Rankings
Abstract
Systemic administration of 3-nitropropionic acid (3-NPA) is commonly used to induce Huntingtons disease (HD)-like symptoms in experimental animals. Here, the potential neuroprotective efficiency of rutin and selenium (RSe) co-administration on 3-NPA-induced HD-like symptoms model in mice was investigated. 3-NPA injection evoked severe alterations in redox status, as indicated via increased striatal malondialdehyde and nitric oxide levels, accompanied by a decrease in levels of antioxidant molecules including glutathione, glutathione peroxidase, glutathione reductase, superoxide dismutase, and catalase. Moreover, 3-NPA potentiated inflammatory status by enhancing the production of interleukin-1?, tumor necrosis factor-?, and myeloperoxidase activity. Pro-apoptotic cascade was also recorded in the striatum as evidenced through upregulation of cleaved caspase-3 and Bax, and downregulation of Bcl-2. 3-NPA activated astrocytes as indicated by the upregulated glial fibrillary acidic protein and inhibited brain-derived neurotrophic factor. Furthermore, perturbations in cholinergic and monoaminergic systems were observed. RSe provided neuroprotective effects by preventing body weight loss, oxidative stress, neuroinflammation, and the apoptotic cascade. RSe inhibited the activation of astrocytes, increased brain-derived neurotrophic factor, and improved cholinergic and monoaminergic transmission following 3-NPA intoxication. Taken together, RSe co-administration may prevent or delay the progression of HD and its associated impairments through its antioxidant, anti-inflammatory, anti-apoptotic, and neuromodulatory effects. 2019, Springer Science+Business Media, LLC, part of Springer Nature.
Description
Scopus
Keywords
Apoptosis, Brain-derived neurotrophic factor, Glial fibrillary acidic protein, Huntingtons disease, Neuroinflammation, Oxidative stress, 3 nitropropionic acid, brain derived neurotrophic factor, caspase 3, catalase, glial fibrillary acidic protein, glutathione, glutathione peroxidase, glutathione reductase, interleukin 1beta, malonaldehyde, myeloperoxidase, nitric oxide, protein Bax, protein bcl 2, rutoside, selenium, selenium nitrate, superoxide dismutase, tumor necrosis factor, unclassified drug, adult, animal experiment, animal model, animal tissue, antiapoptotic activity, antiinflammatory activity, antioxidant activity, apoptosis, Article, astrocyte, body weight loss, cholinergic system, controlled study, corpus striatum, down regulation, Huntington chorea, male, monoaminergic system, mouse, nervous system inflammation, neuromodulation, neuroprotection, neurotoxicity, nonhuman, oxidation reduction state, oxidative stress, priority journal, upregulation