Evidence map›Paper›PMID 32303785›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2020

Carvacrol reduces hippocampal cell death and improves learning and memory deficits following lead-induced neurotoxicity via antioxidant activity.

Fatemeh Zare Mehrjerdi, Somayeh Niknazar, Maryam Yadegari, Fatemeh Ali Akbari, Zeynab Pirmoradi, Mehdi Khaksari

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Review
  6. The effects of carvacrol and p-cymene on AβCNS neuroscience & therapeutics · 2024
    Article
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  9. Antidepressant-like effect of endogenous SONaunyn-Schmiedeberg's archives of pharmacology · 2023
    Article
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  11. Review
  12. 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

6 authors at 3 institutions in 1 country.

Fatemeh Zare MehrjerdiNeurobiomedical Research Center, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran.
Somayeh NiknazarHearing Disorders Research Center, Loghman Hakim Medical Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Maryam YadegariNeurobiomedical Research Center, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran.
Fatemeh Ali AkbariNeurobiomedical Research Center, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran.
Zeynab PirmoradiNeurobiomedical Research Center, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran.
Mehdi KhaksariSchool of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran. Khaksari417@yahoo.com.
Shahid Sadoughi University of Medical Sciences and Health Services · IRShahid Beheshti University of Medical Sciences · IRShahroud University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Carvacrol is a monoterpene with neuroprotective effects in several animal models of neurodegeneration, including epilepsy, ischemia, and traumatic neuronal events. In this study, we aimed to examine the effects of carvacrol on neurodegeneration induced by lead acetate in rats. A total of 50 male Wistar rats were divided into five equal groups. The control group received drinking water, while the neurotoxic group was exposed to 500 ppm of lead acetate in drinking water for 40 days. The three remaining groups, which were also exposed to 500 ppm of lead acetate, received carvacrol at doses of 25, 50, and 100 mg/kg orally for 40 days. The Morris water maze test was employed to examine spatial learning and memory. Pathological damage to the hippocampus was determined by Nissl staining. The level of malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) were detected using biochemical analysis and the free radical scavenging activity as evaluated by the DPPH test. Administration of carvacrol significantly restored learning and memory impairment induced by lead acetate. Moreover, carvacrol ameliorated neurodegeneration, antioxidative capacity, and lipid peroxidation in the hippocampus of rats exposed to lead. The present results provide a rationale for the inhibitory role of carvacrol in the attenuation of lead-induced neurotoxicity.

Indexed as

AnimalsAntioxidantsCatalaseCell DeathCymenesDose-Response Relationship, DrugHippocampusLipid PeroxidationMaleMalondialdehydeMaze LearningMemory DisordersNeuroprotective AgentsNeurotoxicity SyndromesOrganometallic CompoundsRatsAntioxidantscarvacrolCatalaseCymeneslead acetateMalondialdehydeNeuroprotective AgentsOrganometallic CompoundsSuperoxide DismutaseCarvacrolLead acetateLearning and memoryNeurotoxicityOxidative stress

Identifiers

PMID32303785
OpenAlexW3016523068

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.