Evidence mapPaperPMID 40534331Full record

ArticleJournal of biochemical and molecular toxicology2025

Protective Effects of Chrysin Against Diclofenac-Induced Nephrotoxicity in Rats via Attenuation of Oxidative Stress, Apoptosis and Endoplasmic Reticulum Stress.

Cuneyt Caglayan, İzzettin Ekinci, Cihan Gur, Adnan Ayna, İbrahim Bayav, Fatih Mehmet Kandemir

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Article in Journal of biochemical and molecular toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

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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.

Cuneyt CaglayanDepartment of Medical Biochemistry, Faculty of Medicine, Bilecik Şeyh Edebali University, Bilecik, Türkiye.ORCID https://orcid.org/0000-0001-5608-554X
İzzettin EkinciVocational School of Health Services, Bingol University, Bingol, Türkiye.ORCID https://orcid.org/0000-0003-0418-6773
Cihan GurDepartment of Medical Laboratory Techniques, Vocational School of Health Services, Atatürk University, Erzurum, Türkiye.ORCID https://orcid.org/0000-0001-6775-7858
Adnan AynaDepartment of Chemistry, Faculty of Science and Literature, Bingol University, Bingol, Türkiye.ORCID https://orcid.org/0000-0001-6801-6242
İbrahim BayavDepartment of Medical Biology, Faculty of Medicine, Pamukkale University, Denizli, Türkiye.
Fatih Mehmet KandemirDepartment of Medical Biochemistry, Faculty of Medicine, Aksaray University, Aksaray, Türkiye.

Funding

The authors received no specific funding for this work.
6 · The paper itself

Abstract

Diclofenac (DCL) is a broadly prescribed non-steroidal anti-inflammatory drug (NSAID) for pain management and has been linked to nephrotoxicity despite its therapeutic benefits. This study provides new insights into the palliative impacts of chrysin (CH) against DCL-induced kidney damage by modulating oxidative injury, endoplasmic reticulum (ER) stress and apoptosis. The rats were divided into five groups: the control group (Group 1), CH-only group (50 mg/kg, Group 2), DCL-only group (50 mg/kg, Group 3), DCL + CH (25 mg/kg, Group 4), and DCL + CH (50 mg/kg, Group 5). DCL injection led to significant renal damage marked by elevated serum urea, creatinine and malondialdehyde (MDA) levels, reduced glutathione (GSH) concentration, and decreased activities of antioxidant enzymes (glutathione peroxidase, superoxide dismutase and catalase). The mRNA expression levels of Ho-1 and Nrf2 were also suppressed. Additionally, DCL treatment triggered apoptosis as evidenced by increased expression of Bax and caspase-3 alongside decreased Bcl-2 expression. Furthermore, DCL induced ER stress was confirmed by upregulation of Perk, Ire1, Atf-6, and Grp78 transcription levels. Also, it was demonstrated that DCL treatment upregulated Mmp2 and Mmp9 levels. Treatment with CH significantly mitigated these adverse effects suggesting that CH effectively protects DCL-induced kidney toxicity by targeting multiple pathways. In summary, this study highlights the importance of CH as a promising therapeutic agent for alleviating kidney damage associated with DCL toxicity.

Indexed as

ApoptosisDiclofenacEndoplasmic Reticulum StressFlavonoidsKidneyKidney DiseasesOxidative StressAnimalsMaleRatsRats, Sprague-DawleychrysinDiclofenacFlavonoidsapoptosischrysindiclofenacendoplasmic reticulum stressnephrotoxicity

Identifiers

PMID40534331
PMCPMC12177443

What Socratic holds

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Registered trials

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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 Socratic graph.