Protective Effects of Morin Against Paracetamol-Induced Nephrotoxicity via Modulation of Oxidative Stress, Inflammation, and Apoptosis Pathways

Objective: Paracetamol (PCM), although a widely used and non-prescription effective analgesic and antipyretic, can cause nephrotoxicity by causing kidney damage at high doses. Morin (MRN) is a flavonoid found in white mulberry and cranberry, with low toxicity and prominent antioxidant, anti-inflammatory, and antiapoptotic properties. This study aimed to investigate the effects of MRN on PCM-induced kidney toxicity by biochemical, molecular, and histopathological methods. Materials-Methods: Thirty-five Wistar rats were divided into Control, MRN (100 mg/kg), PCM (1000 mg/kg), PCM+MRN50 (50 mg/kg), and PCM+MRN100 (100 mg/kg) groups (n=7); the substances were administered orally for 6 days. The blood and kidney tissues were evaluated with biochemical (urea, creatinine, MDA, GSH, SOD, CAT, GPx), genetic (NF-κB, TNF-α, Caspase-3, Bax, Bcl-2, KIM-1, AQP2) and histopathological methods. Results: While PCM negatively affected kidney function tests, oxidative stress levels, inflammation, and apoptosis markers and caused kidney damage, MRN suppressed these negative effects at both doses, improved kidney function, antioxidant defense, inflammation, and apoptosis parameters, and reduced histopathological damage. Conclusion: The study found that MRN effectively protected kidney tissue from PCM-induced damage by reversing oxidative stress, inflammation, and apoptosis.