Background: Renal toxicity remains a significant challenge in clinical pharmacology, often resulting from adverse drug effects such as those caused by cimetidine, a commonly used H₂ receptor antagonist. While effective in managing gastrointestinal conditions, prolonged or high-dose cimetidine administration has been linked to renal impairment, characterized by histopathological damage and alterations in biochemical markers. This study investigates the potential nephro-protective effects of beetroot (Beta vulgaris L.), a nutrient-rich plant known for its antioxidant properties, against cimetidine-induced renal injury. Methods: Thirty-five male Wistar rats were allocated into seven groups to receive various treatments, including cimetidine alone, beetroot extract at different doses, and combinations thereof, over a seven-week period. Results: Histological examinations revealed that cimetidine caused significant renal damage, including hemorrhage, necrosis, and fibrosis, which were notably ameliorated by beetroot supplementation, especially at higher doses. Biochemical analyses demonstrated that beetroot significantly mitigated oxidative stress markers such as malondialdehyde (MDA) relative to the untreated group (p-value 0.001); it also significantly preserved functional parameters including serum creatinine (p value 0.001) and lactate dehydrogenase (LDH) (p-value 0.003) compared to the untreated rats. Conclusion: The findings suggest that beetroot exerts protective effects through its anti-oxidative and anti-fibrotic properties, attenuating cimetidine-induced nephrotoxicity. These results highlight the potential of natural bioactive compounds like beetroot as adjuncts to prevent or reduce drug-induced renal injury, warranting further molecular investigations and clinical validation.
Oladimeji et al. (Wed,) studied this question.