Evidence map›Paper›PMID 35699857›Full record

ArticleMetabolic brain disease2022

Neuroprotective effects of 18β-glycyrrhetinic acid against bisphenol A-induced neurotoxicity in rats: involvement of neuronal apoptosis, endoplasmic reticulum stress and JAK1/STAT1 signaling pathway.

Cuneyt Caglayan, Fatih Mehmet Kandemir, Adnan Ayna, Cihan Gür, Sefa Küçükler, Ekrem Darendelioğlu

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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 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
9.0field-weighted citation impact, top 1% 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

28 citing papers in PubMed, 59 citations in OpenAlex.

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  17. Glycyrrhizic Acid Alleviates Semen Strychni-Induced Neurotoxicity Through the Inhibition of HMGB1 Phosphorylation and Inflammatory Responses.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
    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.

Cuneyt CaglayanDepartment of Biochemistry, Faculty of Veterinary Medicine, Bingol University, 12000, Bingol, Turkey. ccaglayan@bingol.edu.tr.ORCID 0000-0001-5608-554X
Fatih Mehmet KandemirDepartment of Medical Biochemistry, Faculty of Medicine, Aksaray University, Aksaray, Turkey.
Adnan AynaDepartment of Chemistry, Faculty of Science and Literature, University Bingol, 12000, Bingol, Turkey.
Cihan GürDepartment of Biochemistry, Faculty of Veterinary Medicine, Atatürk University, 25240, Erzurum, Turkey.
Sefa KüçüklerDepartment of Biochemistry, Faculty of Veterinary Medicine, Atatürk University, 25240, Erzurum, Turkey.
Ekrem DarendelioğluDepartment of Molecular Biology and Genetics, Faculty of Science and Literature, University Bingol, 12000, Bingol, Turkey.
Bingöl University · TRAtatürk University · TRAksaray University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The exposure to bisphenol A (BPA) is inevitable owing to its common use in the production of polycarbonate plastics. Studies to reduce side effects are gaining importance since BPA causes severe toxicities in important tissues such as testes, lungs, brain, liver and kidney. The current study was planned to study ameliorative effect of 18β-glycyrrhetinic acid (18β-GA) on BPA induced neurotoxicity. Fourty Wistar albino rats were divided into five equal groups as follows: I-Control group, II-18β-GA group (100 mg/kg), III- BPA group (250 mg/kg), IV-250 mg/kg BPA + 50 mg/kg 18β-GA group, V-250 mg/kg BPA + 100 mg/kg 18β-GA group. BPA intoxication was associated with increased MDA level while reduced GSH concentration, activities of glutathione peroxidase, superoxide dismutase, and catalase. BPA supplementation caused apoptosis in the brain by up-regulating caspase-3 and Bax levels and down-regulating Bcl-2. BPA also caused endoplasmic reticulum (ER) stress by increasing mRNA transcript levels of PERK, IRE1, ATF-6 and GRP78. Additionally, it was observed that BPA administration activated JAK1/STAT1 signaling pathway and levels of TNF-α, NF-κB, p38 MAPK and JNK in the brain. However, co-treatment with 18β-GA at a dose of 50 and 100 mg/kg considerably ameliorated oxidative stress, inflammation, apoptosis, ER stress and JAK1/STAT1 signaling pathway in brain tissue. Overall, the data of this study indicate that brain damage associated with BPA toxicity could be ameliorated by 18β-GA administration.

Indexed as

Endoplasmic Reticulum StressNeuroprotective AgentsAnimalsApoptosisBenzhydryl CompoundsBisphenol A CompoundsGlycyrrhetinic AcidOxidative StressPhenolsRatsRats, WistarSignal TransductionSTAT1 Transcription Factor18alpha-glycyrrhetinic acidBenzhydryl Compoundsbisphenol ABisphenol A CompoundsGlycyrrhetinic AcidNeuroprotective AgentsPhenolsStat1 protein, ratSTAT1 Transcription Factor18β-glycyrrhetinic acidBisphenol AEndoplasmic reticulum stressJAK1/STAT1 signaling pathwayOxidative stress

Identifiers

PMID35699857
OpenAlexW4282828259

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.