Syzygium aromaticum water extract attenuates ethanol-induced gastric injury through antioxidant effects in rats

Abstract

Abstract. The aim of the present study was to investigate whether Syzygium aromaticum water extract (SAWE) has a protective effect against ethanol-induced gastric injury in rats. Acute gastric injury was induced via intragastric administration of absolute ethanol at a dose of 5 ml/kg. SAWE (250 or 500 mg/kg/day) or cimetidine (100 mg/kg/day), which was used as a positive control, were administered to the rats 2 h prior to ethanol administration for 3 days. All rats were sacrificed 24 h following the final ethanol administration. To examine whether SAWE has a gastroprotective effect, assays were performed to assess the contents of malondialdehyde (MDA) and glutathione (GSH), the activities of catalase, glutathione-S-transferase and superoxide dismutase, and an immune-linked immunosorbent assay was performed for prostaglandin E 2 (PGE 2 ) production in gastric tissues by hematoxylin and eosin and periodic acid-Schiff staining. Histological assessment of the gastric wall was performed. Compared with ethanol treatment alone, treatment with SAWE at a dose of 250 mg/kg/day significantly decreased the gastric MDA content and increased the GSH content, catalase activity, and production of gastric PGE 2 . Histological assessment showed that SAWE attenuated inflammatory cell infiltration and the loss of epithelial cells. These findings suggested that SAWE protected against ethanol-induced gastric mucosal injury in the rats. These effects appeared to be associated with antioxidant activity, activation of the production of PGE 2 , suppression of inflammatory cell infiltration and loss of epithelial cells in the gastric mucosa. Collectively, SAWE may be beneficial in the prevention of gastric disease associated to oxidative stress.

The Gastroprotective Effect of Small Molecule Oligopeptides Isolated from Walnut (Juglans regia L.) against Ethanol-Induced Gastric Mucosal Injury in Rats

“…Most studies of ethanol-induced gastric mucosal damage have been performed in rodent models, but there is no generally accepted gavage dose of alcohol to date. According to multiple pieces of literature, absolute ethanol administered at a dose of 5 mL/kg in rodents was used more frequently, and the gastric mucosa injury can occur about 30 min and generally reach a peak 60 min after alcohol intake, which took into account differences in alcohol metabolism between rodents and humans [8,[25][26][27][28]. In pre-experiments, we found that the dose of absolute ethanol caused obvious damage to gastric mucosa with low mortality of rats.…”

“…At day 30, after the final administration, all rats were fasted for 24 h but given free access to water. Then rats were gavage with absolute ethanol at 5 mL/kg body weight to induce gastric ulceration based on reference to other research and pre-experiment [8,[25][26][27][28]. One hour later, animals were sacrificed, a blood sample was collected from the femoral artery and then centrifuged at 3000 rpm for 15 min to obtain serum and preserved at −80 • C; the stomach was immediately removed, and the gastric juice was collected into a tube and then the pH of gastric content was recorded with a digital pH meter.…”

Gastro-protective actions of Aloe barbadensis Miller mitigate ethanol-induced gastric injury in rats

“…The secretion of bicarbonate into adherent layer of mucus gel creates pH gradient with a nearneutral pH at the epithelial surfaces in the stomach and duodenum, thereby providing first line of mucosal protection against luminal acid. Perturbation of the mucus-bicarbonate barrier adversely affects the mucosa and leads to loss of epithelial cells [21]. In gastric mucosa, ethanol causes gastritis via lipid peroxidation.…”

Protective Effects of Small-Molecule Oligopeptides Isolated from Tilapia Fish Scale on Ethanol-Induced Gastroduodenal Injury in Rats

“…It was found that 5 mL/kg of anhydrous ethanol could cause significant damage to the gastroduodenal mucosa without causing death in rats. Therefore, an acute gastroduodenal injury model was established with this dose [ 26 , 39 ].…”