Investigation of the preventive action of rebamipide versus cadmium nephrotoxicity effect in rats

Cadmium (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.

This study aimed to investigate the potential reno-protective effects of rebamipide against cadmium-induced nephrotoxicity.

Fifty 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.

Cadmium 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.

Rebamipide acts as a promising preventive agent against cadmium-induced nephrotoxicity, through its potent antioxidant and anti-inflammatory mechanisms.