Evidence map›Paper›PMID 32215265›Full record

ArticleInternational journal of molecular and cellular medicine2019

Protective Effect of Naringin on Bisphenol A-Induced Cognitive Dysfunction and Oxidative Damage in Rats.

Masoud Mahdavinia, Akram Ahangarpour, Leila Zeidooni, Azin Samimi, Saeid Alizadeh, Mohammad Amin Dehghani, Soheila Alboghobeish

Open access · greenAbstract read
In one paragraph

Article in International journal of molecular and cellular medicine, 2019. 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
2.0field-weighted citation impact, top 15% 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, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Can Antioxidants Reduce the Toxicity of Bisphenol?Antioxidants (Basel, Switzerland) · 2022
    Review
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 1 institution in 1 country.

Masoud MahdaviniaDepartment of Pharmacology and Toxicology, School of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Akram AhangarpourHealth Research Institute, Diabetes Research Center, Department of Physiology, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Leila ZeidooniDepartment of Toxicology, School of Pharmacy, Student Research Committee of Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Azin SamimiDepartment of Toxicology, School of Pharmacy, Student Research Committee of Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Saeid AlizadehDepartment of Toxicology, School of Pharmacy, Student Research Committee of Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Mohammad Amin DehghaniDepartment of Toxicology, School of Pharmacy, Student Research Committee of Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Soheila AlboghobeishDepartment of Pharmacology, School of Medicine, Jundishapur University of Medical Sciences, Ahvaz, Iran.
Ahvaz Jundishapur University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bisphenol A (BPA) is one of the highest volume chemicals produced worldwide, which is used in many plastic industries. The present study aimed to evaluate the effect of BPA on cognitive functions and oxidative stress, and determine whether the naringin (NG) co-administration can modify the effect of this compound on cognitive functions and inhibit any possible oxidative stress in the brain tissue of rats. Adult male Wistar rats were divided into six groups. Group I: control, Group II: BPA-treated rats (50 mg/kg/day), Group III, IV, V: BPA+NG (40, 80, 160 mg/kg/day), Group VI: NG (160 mg/kg/day) alone. Cognitive functions were evaluated using step-down latency (SDL) on a passive avoidance apparatus, and transfer latency (TL) in elevated plus-maze. A significant decrease in SDL, prolongation of TL, noticeable oxidative impairment and increase in acetylcholinesterase activity were observed in the BPA-treated in comparison with the control group. Also, the co-administration of NG (160 mg/kg) antagonized the effect of BPA on SDL and TL, attenuated oxidative damage by lowering malondialdehyde and nitrite concentrations and restored superoxide dismutase, catalase, and glutathione S-transferase activities. On the other hand, acetylcholinesterase activity was reduced in the groups co-administred with NG (80 or 160 mg/kg) and BPA in comparison with the BPA alone-treated group. The present study highlighted the therapeutic potential of NG against BPA-induced cognitive impairment and oxidative damage.

Indexed as

Bisphenol Acognitive dysfunctionnaringinoxidative stress

Identifiers

PMID32215265
PMCPMC7081084
OpenAlexW2983682764

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.