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Protective role of melatonin against diclofenac-induced acute kidney injury
Sahar Mohamed El Agaty1, Sherif Khedr2, Doaa Karem Metwaly Mostafa3
1Department of Medical Physiology, Faculty of Medicine, Ain Shams University, Cairo, Egypt; Department of Medical Physiology, Faculty of Medicine, Galala University, Suez, Egypt; Basic Medical Sciences Department, Faculty of Pharmacy, King Salman International University, Sinai, Egypt.
Abstract:
Diclofenac (DF), a non-steroidal anti-inflammatory drug, is commonly used to relieve pain and inflammation. High doses of DF might induce acute kidney injury (AKI), particularly in elderly, a known vulnerable population.
Aim:
We aimed to assess the protective role of melatonin (Mel) on DF-induced AKI in aged rats and to highlight the underpinning mechanisms include, oxidative stress and inflammation focusing on microRNA-34a (miR-34a), nuclear factor erythroid-2-related factor-2/hemeoxygenase-1 (Nrf2/HO-1) and NLR family-pyrin domain containing-3 (NLRP3) inflammasome pathways, and to elucidate the possibility of epithelial sodium channel (ENaC) involvement.
Materials And Methods:
Thirty old male Wistar rats were allocated randomly into 3 groups: Control, DF and Mel-DF groups.
Key Findings:
Melatonin provided nephroprotective effects against DF-induced AKI via attenuating the expression of renal miR-34a and subsequently promoting the signaling of Nrf2/HO-1 with elevation of the antioxidant defense capacity and suppressing NLRP3 inflammasomes. Melatonin alleviated DF-induced hypernatremia via decreasing the ENaC expression. Renal histopathological examination revealed significant reduction in vascular congestion, mononuclear infiltration, glomerulo-tubular damage, fibrosis and TNF-α optical density.
Significance:
It can be assumed that melatonin is a promising safe therapeutic agent in controlling DF-induced AKI in elderly.
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