Evaluation of Rosuvastatin and Selenium Effects on TNF- Α and SOD Biomarkers on Indomethacin Induced Peptic Ulcer in Rat Model
DOI:
https://doi.org/10.63278/jicrcr.vi.2584Abstract
Peptic ulcers are lesions resulting from defects in the muscularis mucosae of the gastrointestinal mucosa. These deficiencies may result from cellular regeneration, blood circulation, acid-pepsin secretion, mucus production, mucosal barriers, and internal factors such as epidermal growth hormones and prostaglandins. Despite the availability of numerous pharmacological options for stomach ulcer management, there is an increasing interest in alternative therapies that have less adverse effects for refractory patients. Statins possess antioxidant and anti-inflammatory properties; nevertheless, their anti-ulcerative effects on gastric ulcers remain largely unexplored. Selenium, a trace mineral, is a crucial element of antioxidant enzymes such as glutathione peroxidase, which safeguard cells against oxidative damage. This research evaluated the effects of omeprazole, rosuvastatin, and selenium supplementation on indomethacin-induced gastric ulcers in male albino rats. Animals were categorized into seven groups: carboxymethylcellulose (control group), omeprazole (20 mg/kg), rosuvastatin (20 mg/kg), selenium (200 mcg/kg), a combination of rosuvastatin and omeprazole, and a combination of rosuvastatin and selenium. Thirty minutes post-administration of omeprazole and rosuvastatin, and two hours post-administration of selenium, Indomethacin (60 mg/kg) was given orally to all groups. Four hours later, the animals were euthanized, and the average ulcer indexes for each group were determined. The stomachs were examined histopathologically, and biomarkers were measured.The results indicated the ulcer index as follows: healthy 0±0, indomethacin group 3.3±0.5, omeprazole 0.8±0.4, rosuvastatin 1.3±0.5, selenium 1±0, the first combination group (rosuvastatin & omeprazole) 0.5±0.5, and the combination (rosuvastatin & selenium) 1±0. Concluded that rosuvastatin and selenium expedited ulcer healing by promoting mucosal regeneration, diminishing lipid peroxidation, enhancing antioxidant activity, and altering mucus secretion response.