ArticleIrish journal of medical science2026
Investigation of the preventive action of rebamipide versus cadmium nephrotoxicity effect in rats.
Article in Irish journal of medical science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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Who cites it
2 citing papers in PubMed.
- Berberine Attenuates Cadmium-Induced Nephrotoxicity by Suppressing LDHA-Mediated Glycolytic Reprogramming and Restoring Mitochondrial TCA Cycle Metabolism.Biomolecules · 2026Article
- The role of endoplasmic reticulum stress-mediated autophagy in cadmium-induced liver injury in rats.Frontiers in veterinary science · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCadmium (Cd) is a major environmental and industrial pollutant that exhibits a significant health risk to humans and animals. Renal toxicity is a prevalent adverse effects of cadmium exposure. Rebamipide (REBA) is pharmacological agent known for its potent antioxidants properties.
aimThis study aimed to investigate the potential reno-protective effects of rebamipide against cadmium-induced nephrotoxicity. MAIN
methodsFifty rats were allocated into five groups; (1) a normal control group; (2) cadmium chloride group (5 mg/kg, single dose, i.p.); (3) a group treated with rebamipide (100 mg/kg, p.o.) for nine days (seven days before and two days after a single cadmium dose); (4) a group treated with rebamipide (200 mg/kg, p.o.) for nine days (seven days before and two days after a single cadmium dose); and (5) a group treated with rebamipide only (200 mg/kg, p.o.) for nine days. KEY
findingsCadmium administration significantly increased serum urea, creatinine, and the renal injury marker KIM-1. It also elevated inflammatory mediators, including tumor necrosis factor-α (TNF-α), nuclear factor kappa B (NF-κB), and inducible nitric oxide synthase (iNOS). Concurrently, cadmium halted catalase (CAT), superoxide dismutase (SOD) activities, and reduced glutathione (GSH) level, while increasing malondialdehyde (MDA) content. Furthermore, cadmium dysregulated autophagy, decreasing Beclin-1 and increasing microtubule-associated protein 1 light chain 3 (MAP-LC3) levels. Treatment with rebamipide effectively improved renal histology, reduced inflammatory markers, and restored the balance of all the aforementioned oxidative and autophagic parameters.
conclusionRebamipide acts as a promising preventive agent against cadmium-induced nephrotoxicity, through its potent antioxidant and anti-inflammatory mechanisms.
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