Gastroprotective Effect of Myricetin on Ethanol-Induced Acute Gastric Injury in Rats

The flavonoid myricetin is abundant in vegetables and has various bioactive properties, including anti-inflammatory and antioxidative activities. In the present study, we explored the effects of myricetin on alcohol-induced gastric ulcer in a rat model. To induce gastric ulcer, absolute ethanol (5 mL/kg body weight) was orally administrated to each rat. The positive control and myricetin-treated groups were given oral doses of omeprazole (20 mg/kg) or myricetin (12 mg/kg), respectively, 1 hour prior to the administration of absolute alcohol. We found that pretreatment with myricetin significantly decreased alcohol-induced gastric ulcer, hemorrhage, hyperemia, and epithelial cell loss in the gastric mucosa. Myricetin pretreatment reduced the level of malondialdehyde (MDA) and increased that of total glutathione (GSSG/GSH) and superoxide dismutase (SOD) in gastric tissues. In addition, it elevated the expression levels of cyclooxygenase-1 (COX-1) and prostaglandin E-2 (PGE(2)) and decreased the phosphorylation of nuclear factor kappa B (NF-kappa B). Together, these results indicate that myricetin effectively inhibits ethanol-induced acute gastric injury by preventing oxidative damage, stimulating PGE(2) production, and inhibiting NF-kappa B activation. We suggest that myricetin may be an alternative treatment for gastric injury caused by alcohol intake.

Automated summary

In this study, it was found that pretreatment with myricetin effectively reduced alcohol-induced gastric ulcers and injury in rats by decreasing oxidative damage, increasing PGE(2) production, and inhibiting NF-kappa B activation. Myricetin may be considered as an alternative treatment for gastric injury caused by alcohol consumption.