Evidence map›Paper›PMID 41494743›Full record

ArticleJournal of veterinary science2026

Fulvic acid protects hepatic tissue from amoxicillin/clavulanate-induced hepatotoxicity.

Hasan Mansur Durgun, Eda Yildizhan

Abstract read
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Article in Journal of veterinary science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

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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

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3 · Its place in the literature

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Hasan Mansur DurgunDepartment of Emergency, Dicle University, Faculty of Medicine Hospital, 21280 Sur/Diyarbakır, Turkey.ORCID https://orcid.org/0000-0001-5005-6369
Eda YildizhanDepartment of Histology and Embryology, Dicle University, Faculty of Medicine Hospital, 21280 Sur/Diyarbakır, Turkey. edayildizhan21@gmail.com.ORCID https://orcid.org/0000-0002-5648-6498

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

importanceFulvic acid can protect liver tissue against amoxicillin-clavulanate-induced hepatotoxicity through antioxidant and antiapoptotic effects.

objectiveTo evaluate the protective effects of fulvic acid against amoxicillin-clavulanate-induced hepatotoxicity using biochemical, histopathological, immunohistochemical, functional, and bioinformatic analyses.

methodsTwenty-eight male Wistar rats were randomly assigned to 4 groups (n = 7/group): sham (saline), amoxicillin-clavulanate (10 mg/kg/day), fulvic acid (100 mg/kg/day), and combined treatment. Treatments were administered orally for 21 days. Liver injury and oxidative stress were assessed by serum alanine aminotransferase, aspartate aminotransferase, malondialdehyde, total antioxidant status, and total oxidant status; tissue injury was assessed histologically. Apoptosis was evaluated by immunohistochemistry for BAX and BCL2. Hepatic detoxification capacity was assessed by a caffeine clearance test. In silico analyses predicted molecular targets of fulvic acid and enriched pathways.

resultsAmoxicillin-clavulanate increased transaminases, oxidative stress markers, and proapoptotic signaling and induced vascular congestion and sinusoidal dilatation. Co-treatment with fulvic acid improved serum biomarkers, reduced histological injury, downregulated BAX, and restored BCL2 staining intensity. In silico analysis identified predicted fulvic-acid targets enriched in metabolic and proliferation-related pathways. CONCLUSIONS AND RELEVANCE: Fulvic acid attenuated amoxicillin-clavulanate-induced hepatotoxicity, consistent with antioxidant and antiapoptotic mechanisms. Further studies are warranted to define dose-response relationships and translational potential.

Indexed as

Amoxicillin-Potassium Clavulanate CombinationAnti-Bacterial AgentsBenzopyransChemical and Drug Induced Liver InjuryLiverProtective AgentsAnimalsAntioxidantsApoptosisMaleOxidative StressRatsRats, WistarAmoxicillin-Potassium Clavulanate CombinationAnti-Bacterial AgentsAntioxidantsBenzopyransfulvic acidProtective AgentsantibioticantioxidantsapoptosisLiveroxidative stress

Identifiers

PMID41494743
PMCPMC12891820

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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 OpenQuestion graph.