Evidence map›Paper›PMID 35316447›Full record

ArticleMetabolic brain disease2022

Neuroprotective effects of carvacrol against cadmium-induced neurotoxicity in rats: role of oxidative stress, inflammation and apoptosis.

Mustafa Onur Yıldız, Hamit Çelik, Cuneyt Caglayan, Aydın Genç, Tuba Doğan, Emine Satıcı

Abstract read
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In one paragraph

Article in Metabolic brain disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

9 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  6. Review
  7. The Protective Effect of the Supplementation with an Extract fromInternational journal of molecular sciences · 2024
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  8. Review
  9. A New Target in Inflammatory Diseases: Lycopene.The Eurasian journal of medicine · 2022
    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

6 authors at 3 institutions in 1 country.

Mustafa Onur YıldızDepartment of Neurology, Erzurum Regional Health Application and Research Hospital, Health Sciences University, Erzurum, Turkey.
Hamit ÇelikDepartment of Neurology, Private Buhara Hospital, Erzurum, Turkey.
Cuneyt CaglayanDepartment of Biochemistry, Faculty of Veterinary Medicine, Bingol University, 12000, Bingol, Turkey. ccaglayan@bingol.edu.tr.ORCID http://orcid.org/0000-0001-5608-554X
Aydın GençDepartment of Biochemistry, Faculty of Veterinary Medicine, Bingol University, 12000, Bingol, Turkey.
Tuba DoğanDepartment of Biochemistry, Faculty of Veterinary Medicine, Atatürk University, Erzurum, Turkey.
Emine SatıcıDepartment of Biochemistry, Faculty of Veterinary Medicine, Atatürk University, Erzurum, Turkey.
Atatürk University · TRBingöl University · TRErzurum Regional Training and Research Hospital · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cadmium (Cd), is a heavy metal reported to be associated with oxidative stress and inflammation. In this paper, we investigated the possible protective effects of carvacrol against Cd-induced neurotoxicity in rats. Adult male Sprague Dawley rats were treated orally with Cd (25 mg/kg body weight) and with carvacrol (25 and 50 mg/kg body weight) for 7 days. Carvacrol decreased the levels of malondialdehyde (MDA), glial fibrillary acidic protein (GFAP) and monoamine oxidase (MAO), and significantly increased the levels of glutathione (GSH) and activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) in brain tissue. Additionally, carvacrol alleviated the in levels of inflammation and apoptosis related proteins involving p38 mitogen-activated protein kinase (p38 MAPK), cyclooxygenase-2 (COX-2), nuclear factor kappa B (NF-κB), B-cell lymphoma-3 (Bcl-3), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), myeloperoxidase (MPO), prostaglandin E2 (PGE2), neuronal nitric oxide synthase (nNOS), inducible nitric oxide synthase (iNOS), cysteine aspartate specific protease-3 (caspase-3) and Bcl-2 associated X protein (Bax) in the Cd-induced neurotoxicity. Carvacrol also decreased the mRNA expression of matrix metalloproteinases (MMP9 and MMP13), as well as 8-hydroxy-2'-deoxyguanosine (8 - OHdG) level, a marker of oxidative DNA damage. Collectively, our findings indicated that carvacrol has a beneficial effect in ameliorating the Cd-induced neurotoxicity in the brain of rats.

Indexed as

Neuroprotective AgentsNeurotoxicity SyndromesAnimalsApoptosisBody WeightCadmiumCymenesGlutathioneInflammationMaleOxidative Stressp38 Mitogen-Activated Protein KinasesRatsRats, Sprague-DawleyCadmiumcarvacrolCymenesGlutathioneNeuroprotective Agentsp38 Mitogen-Activated Protein KinasesApoptosisCadmiumCarvacrolInflammationNeurotoxicity

Identifiers

PMID35316447
OpenAlexW4220732545

What OpenQuestion holds

Textmetadata
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.