Mitigation of Ochratoxin A-Induced Renal Toxicity by Kaempferol in Albino Mice

Document Type : Original paper

Authors

1 Department of Biological Sciences, College of Science, King Faisal University, Al-Ahsa, Saudi Arabia.

2 Centre of Molecular Medicine and Diagnostics (COMManD), Department of Biochemistry, Saveetha Dental College & Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai, Tamil Nadu, India.

3 Laboratory of Aromatic and Medicinal Plants, Center of Biotechnology of Borj-Cedria, Technopole of Borj-Cedria, Hammam-Lif, Tunisia.

4 Department of Zoology, Faculty of Science, Alexandria University Egypt, Alexandria, Egypt.

5 Department of Anatomy, College of Veterinary Medicine, King Faisal University, Al-Ahsa, Saudi Arabia.

10.22127/rjp.2024.441154.2348

Abstract

Background and objective: This study investigated the protective effects of kaempferol, a natural flavonoid known for its antioxidant properties, against ochratoxin A-induced renal damage. Ochratoxin A, a nephrotoxic mycotoxin found in contaminated food and feed, primarily induces renal damage through oxidative stress. The objective was to assess kaempferol’s potential in mitigating ochratoxin A -induced renal toxicity and its underlying molecular mechanisms. Methods: Male albino mice were divided into four groups: normal control, kaempferol control, ochratoxin A -induced renal toxicity, and ochratoxin A -induced renal toxicity treated with kaempferol. Ochratoxin A was administered twice a week for 8 weeks at 5 mg/kg body weight to induce renal toxicity. Kaempferol (50 mg/kg) was administered twice a week for 8 weeks after a 4-hour interval following ochratoxin A administration. Results: Results showed that kaempferol normalized levels of blood urea nitrogen (BUN) and creatinine, indicating protection against ochratoxin A-induced pathophysiology. Kaempferol also increased phosphorylation of PI3K and AKT, potentially activating antioxidative and anti-apoptotic signaling pathways regulated by Nrf2. Additionally, kaempferol enhanced Bcl-2 activation while suppressing caspase-3, suggesting anti-apoptotic effects. Histopathological analysis revealed reduced renal damage in kaempferol-treated mice compared to those exposed to ochratoxin A alone. Conclusion: Kaempferol demonstrated efficacy in preventing ochratoxin A -induced kidney injury through antioxidative and anti-apoptotic mechanisms. These findings suggest potential therapeutic applications of kaempferol in oxidative stress-induced renal damage.
 

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