Evidence map›Paper›PMID 31332714›Full record

ArticleNeurotoxicity research2020

Rutin and Selenium Co-administration Reverse 3-Nitropropionic Acid-Induced Neurochemical and Molecular Impairments in a Mouse Model of Huntington's Disease.

Mohamed S Abdelfattah, Sherif E A Badr, Sally A Lotfy, Gouda H Attia, Ahmed M Aref, Ahmed E Abdel Moneim, Rami B Kassab

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Article in Neurotoxicity research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.0field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
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  8. Review
  9. Rutin andFrontiers in veterinary science · 2025
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Mohamed S AbdelfattahNatural Products Research Unit (NPRU), Chemistry Department, Faculty of Science, Helwan University, Cairo, 11795, Egypt.
Sherif E A BadrRegional Center for Food and Feed (RCFF), Agriculture Research Center, Giza, Egypt.
Sally A LotfyNatural Products Research Unit (NPRU), Chemistry Department, Faculty of Science, Helwan University, Cairo, 11795, Egypt.
Gouda H AttiaDepartment of Pharmacognosy, College of Pharmacy, Najran University, Najran, Saudi Arabia.
Ahmed M ArefFaculty of Biotechnology, Modern Sciences and Arts University (MSA), Giza, Egypt.
Ahmed E Abdel MoneimDepartment of Zoology and Entomology, Faculty of Science, Helwan University, Cairo, 11795, Egypt.
Rami B KassabFaculty of Biotechnology, Modern Sciences and Arts University (MSA), Giza, Egypt. ramikassab@mail.muni.cz.ORCID http://orcid.org/0000-0002-1520-1601
Helwan University · EGOctober University of Modern Sciences and Arts · EGAgricultural Research Center · EGNajran University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic administration of 3-nitropropionic acid (3-NPA) is commonly used to induce Huntington's 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-1β, tumor necrosis factor-α, 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.

Indexed as

Animalsbcl-2-Associated X ProteinBrain-Derived Neurotrophic FactorCaspase 3CatalaseCorpus StriatumDown-RegulationDrug SynergismGlial Fibrillary Acidic ProteinGlutathioneGlutathione PeroxidaseGlutathione ReductaseHuntington DiseaseInterleukin-1betaMaleMalondialdehyde3-nitropropionic acidbcl-2-Associated X ProteinBrain-Derived Neurotrophic FactorCaspase 3CatalaseGlial Fibrillary Acidic ProteinGlutathioneGlutathione PeroxidaseGlutathione ReductaseInterleukin-1betaMalondialdehydeNeuroprotective AgentsNitric OxideNitro CompoundsPeroxidasePropionatesProto-Oncogene Proteins c-bcl-2RutinSeleniumSuperoxide DismutaseTumor Necrosis Factor-alphaApoptosisBrain-derived neurotrophic factorGlial fibrillary acidic proteinHuntington’s diseaseNeuroinflammationOxidative stress

Identifiers

PMID31332714
OpenAlexW2963928890

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.