Abdelfattah M.S.Badr S.E.A.Lotfy S.A.Attia G.H.Aref A.M.Abdel Moneim A.E.Kassab R.B.Natural Products Research Unit (NPRU)Chemistry DepartmentFaculty of ScienceHelwan UniversityCairo11795Egypt; Regional Center for Food and Feed (RCFF)Agriculture Research CenterGizaEgypt; Department of PharmacognosyCollege of PharmacyNajran UniversityNajranSaudi Arabia; Faculty of BiotechnologyModern Sciences and Arts University (MSA)GizaEgypt; Department of Zoology and EntomologyFaculty of ScienceHelwan UniversityCairo11795Egypt2020-01-092020-01-09202010298428https://doi.org/10.1007/s12640-019-00086-yPubMedID31332714https://t.ly/kNvKVScopusSystemic 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.EnglishApoptosisBrain-derived neurotrophic factorGlial fibrillary acidic proteinHuntingtons diseaseNeuroinflammationOxidative stress3 nitropropionic acidbrain derived neurotrophic factorcaspase 3catalaseglial fibrillary acidic proteinglutathioneglutathione peroxidaseglutathione reductaseinterleukin 1betamalonaldehydemyeloperoxidasenitric oxideprotein Baxprotein bcl 2rutosideseleniumselenium nitratesuperoxide dismutasetumor necrosis factorunclassified drugadultanimal experimentanimal modelanimal tissueantiapoptotic activityantiinflammatory activityantioxidant activityapoptosisArticleastrocytebody weight losscholinergic systemcontrolled studycorpus striatumdown regulationHuntington choreamalemonoaminergic systemmousenervous system inflammationneuromodulationneuroprotectionneurotoxicitynonhumanoxidation reduction stateoxidative stresspriority journalupregulationArticlehttps://doi.org/10.1007/s12640-019-00086-yPubMedID31332714