Myricetin alleviates indomethacin-induced gastric ulcers in rats via antioxidant, anti-inflammatory and antiapoptotic mechanisms

Gastric ulcers are among the most widespread gastrointestinal diseases, often caused by NSAIDs. Natural compounds with less toxicity and more safety are being explored to minimize their impact. The main goal is to examine the gastroprotective effects of Myricetin in indomethacin-induced gastric ulcers in rats, and the mechanism involved. The rats were allocated into control, negative, standard, Myricetin 10 mg/kg, and Myricetin 20 mg/kg groups. The effect of Myricetin on indomethacin–induced ulcers was examined for 14 days. The Ulcer index, gastric acidity, and PGE₂ level were evaluated. The inflammatory markers (IL-1β, IL-6, and TNF-α), oxidative stress levels (MDA, GSH, CAT, and SOD), histological study, and apoptotic markers (Bax, NF-κB, and caspase-3) were also assessed. Pre-treatment with Myricetin showed a protective effect towards indomethacin-induced gastric ulceration via reducing Ulcer index, gastric juice volume, and increasing gastric pH, and protective PGE₂ level. It also alleviated the level of TNF-α, IL-1β, and IL-6 and modulated MDA, GSH, CAT, and SOD activity and the apoptotic markers (BAX, Caspase-3, and NF-κB) in the gastric mucosa. It was also examined by histopathological study that Myricetin reduced mucosal ulcers, inflammatory infiltration, and degeneration of cell membranes. The results showed that Myricetin has a gastroprotective effect on indomethacin-induced gastric ulcers through anti-inflammatory, antioxidant, and antiapoptotic mechanisms that should be further investigated.