Evidence map›Paper›PMID 35639233›Full record

ArticleInflammopharmacology2022

Diapocynin neuroprotective effects in 3-nitropropionic acid Huntington's disease model in rats: emphasis on Sirt1/Nrf2 signaling pathway.

Weam W Ibrahim, Nora O Abdel Rasheed

Abstract read
In one paragraph

Article in Inflammopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Mechanistic insights on the role of Nrf-2 signalling in Huntington's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. The Role of NRF2 in Trinucleotide Repeat Expansion Disorders.Antioxidants (Basel, Switzerland) · 2024
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. A supercritical oil extract ofFrontiers in pharmacology · 2024
    Article
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

2 authors.

Weam W IbrahimDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Kasr El Aini St., Cairo, 11562, Egypt. weam.wadie@pharma.cu.edu.eg.ORCID http://orcid.org/0000-0002-4713-0318
Nora O Abdel RasheedDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Kasr El Aini St., Cairo, 11562, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimHuntington's disease (HD) is a rare inherited disease portrayed with marked cognitive and motor decline owing to extensive neurodegeneration. NADPH oxidase is considered as an important contributor to the oxidative injury in several neurodegenerative disorders including HD. Thus, the present study explored the possible neuroprotective effects of diapocynin, a specific NADPH oxidase inhibitor, against 3-nitropropionic acid (3-NP) model of HD in rats.

methodsAnimals received diapocynin (10 mg/kg/day, p.o), 30 min before 3-NP (10 mg/kg/day, i.p) over a period of 14 days.

resultsDiapocynin administration attenuated 3-NP-induced oxidative stress with significant increase in reduced glutathione, glutathione-S-transferase, nuclear factor erythroid 2-related factor 2, and brain-derived neurotrophic factor striatal contents contrary to NADPH oxidase (NOX2; gp91phox subunit) diminished expression. Moreover, diapocynin mitigated 3-NP-associated neuroinflammation and glial activation with prominent downregulation of nuclear factor-Кβ p65 and marked decrement of inducible nitric oxide synthase content in addition to decreased immunoreactivity of ionized calcium binding adaptor molecule 1 and glial fibrillary acidic protein; markers of microglial and astroglial activation, respectively. Treatment with diapocynin hindered 3-NP-induced apoptosis with prominent decrease in tumor suppressor protein and Bcl-2-associated X protein contents whereas the anti-apoptotic marker; B-cell lymphoma-2 content was noticeably increased. Diapocynin neuroprotective effects could be attributed to silent information regulator 1 upregulation which curbed 3-NP-associated hazards resulting in improved motor functions witnessed during open field, rotarod, and grip strength tests as well as attenuated 3-NP-associated histopathological derangements.

conclusionThe present findings indicated that diapocynin could serve as an auspicious nominee for HD management.

Indexed as

Huntington DiseaseNeuroprotective AgentsAcetophenonesAnimalsbcl-2-Associated X ProteinBiphenyl CompoundsBrain-Derived Neurotrophic FactorCalciumGlial Fibrillary Acidic ProteinGlutathioneNADPH OxidasesNF-E2-Related Factor 2Nitric Oxide Synthase Type IINitro CompoundsPropionatesRats3-nitropropionic acidAcetophenonesbcl-2-Associated X ProteinBiphenyl CompoundsBrain-Derived Neurotrophic FactorCalciumdiapocyninGlial Fibrillary Acidic ProteinGlutathioneNADPH OxidasesNeuroprotective AgentsNF-E2-Related Factor 2Nitric Oxide Synthase Type IINitro CompoundsPropionatesSirt1 protein, ratSirtuin 1TransferasesTumor Suppressor Proteins3-nitropropionic acidDiapocyninHuntington's diseaseNADPH oxidaseNrf2Sirt1

Identifiers

PMID35639233
PMCPMC9499906

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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.