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Ulcerative colitis (UC) is a chronic inflammatory bowel disease associated with persistent inflammation, oxidative stress, and epithelial apoptosis. Nicardipine, a dihydropyridine calcium channel blocker, exhibits anti-inflammatory and anti-apoptotic properties, but its therapeutic potential in UC remains unclear. This study evaluated the effects of nicardipine on dextran sulfate sodium (DSS)-induced colitis in mice, focusing on inflammatory, oxidative, and apoptotic pathways. Fifty BALB/c mice were assigned to five groups (n = 10): control, DSS, nicardipine 12 mg/kg, nicardipine 24 mg/kg, and 5-aminosalicylate (ASA) 75 mg/kg. Treatments were administered for 3 days before and 10 days during DSS exposure. Disease severity was assessed by bo
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