Evidence map›Paper›PMID 39867825›Full record

ArticleCytotechnology2025

In vitro and in vivo evidence of the effectiveness of gallic acid on glycerol-induced acute kidney injuries.

Khojasteh Hoseinynejad, Zahra Tafazzoli, Fereshteh Nejaddehbashi, Mehrnoosh Moosavi, Zahra Mansouri

Abstract read
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Article in Cytotechnology, 2025. 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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1 · What the graph read from it

What it found

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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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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Khojasteh HoseinynejadCellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Zahra TafazzoliCellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Fereshteh NejaddehbashiCellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Mehrnoosh MoosaviDepartment of Toxicology, Faculty of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Zahra MansouriCellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Because acute kidney injuries (AKI) are one of the critical health problems worldwide, studies on the risk factors, mechanisms, and treatment strategies seem necessary. Glycerol (GLY), known to induce cell necrosis via myoglobin accumulation in renal tubules, is widely used as an AKI model. This study aimed to evaluate the protective effects of gallic acid (GA) against GLY-induced AKI. The study utilized both in vivo and in vitro models. In vivo, healthy rats were divided into six groups: control (normal saline), GLY (10 mg/kg, intramuscularly), GLY + GA10 (10 mg/kg), GLY + GA50 (50 mg/kg), GLY + GA100 (100 mg/kg), and GA (100 mg/kg). GA was administered by gavage for seven consecutive days, followed by a single intramuscular injection of GLY. Kidney biomarkers, lactate dehydrogenase (LDH), oxidative stress markers, inflammatory indices, and histological parameters were assessed 72 h post-injection. In vitro, human embryonic kidney 2 (HK-2) cells were incubated with GLY and GA at different concentrations (30, 60, and 125 μg/ml) to evaluate cell viability, reactive oxygen species (ROS) production, oxidative stress, and inflammatory cytokines. GLY administration significantly elevated renal dysfunction markers, including blood urea nitrogen and creatinine, alongside oxidative stress and reduced cell viability. GA treatment improved kidney biomarkers, enhanced antioxidant enzyme activity, and reduced inflammatory cytokines. Histological analyses also showed improved kidney structural integrity in GA-treated rats compared to the GLY group. This study confirmed that GLY induces AKI through oxidative stress, inflammation, and structural damage. GA exhibited significant renal protective effects by enhancing antioxidant defenses and reducing inflammation. These findings support GA as a potential natural supplement for preventing or treating renal diseases.

Indexed as

Acute kidney injuryGallic acidGLYInflammationOxidative stress

Identifiers

PMID39867825
PMCPMC11759744

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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.