Document Type : Original Research Article
Authors
1
Department of Medical Biochemistry, Faculty of Basic Medical Sciences, Alex-Ekwueme Federal University, Ndufu-Alike, Ikwo, Ebonyi State.
2
Department of Anatomy, Faculty of Basic Medical Sciences, College of Medicine, Afe Babalola University, Ado-Ekiti, Ekiti State, Nigeria
3
Department of Anatomy, Faculty of Basic Medical Sciences, College of Medicine, Alex-Ekwueme Federal University, Ndufu-Alike, Ikwo, Ebonyi State, Nigeria.
4
Department of Biochemistry, Faculty of Science, Alex-Ekwueme Federal University, Ndufu-Alike, Ikwo, Ebonyi State, Nigeria.
5
Ministry of Agriculture and Rural Development, Ebonyi State Agricultural Development Programme, Abakaliki, Nigeria
Abstract
Objective: Diclofenac is a non-steroidal anti-inflammatory drug linked with considerable organ toxicity caused via increased generation of reactive oxygen species. We evaluated whether the antioxidant effect of virgin coconut oil (VCO) could prevent diclofenac-induced oxidative nephrotoxicity in rats.
Materials and Methods: Randomized rats were pre-supplemented orally with VCO (5 or 10 ml/kg body weight) from day 1 to 24, and injected with normal saline or diclofenac (100 mg/kg) from day 22 to day 24 intraperitoneally.
Results: Diclofenac significantly (p<0.05) increased serum urea and creatinine levels. Renal tumor necrosis factor-α (TNF-α) and malondialdehyde (MDA) levels markedly (p<0.05) increased, whereas renal glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD) activities considerably (p<0.05) decreased compared to normal control. Histopathological alterations were caused by diclofenac. However, treatment with oral VCO for 21 days prior to diclofenac administration, attenuated histological renal damage, and restored antioxidant enzyme activities and TNF-α levels in kidney.
Conclusion: These findings revealed that VCO has potential benefits to prevent diclofenac-induced nephrotoxic damage.
Keywords
)