Abstract
This study was performed to evaluate the protective effect and safety of Oryeongsan water extract (OSWE) on ethanol-induced acute gastric mucosal injury and an acute toxicity study in rats. Acute gastric lesions were induced via intragastric oral administration of absolute ethanol at a dose of 5 mL/kg. OSWE (100 and 200 mg/kg) was administered to rats 2 h prior to the oral administration of absolute ethanol. The stomach of animal models was opened and gastric mucosal lesions were examined. Gastric mucosal injuries were evaluated by measuring the levels of malondialdehyde (MDA), glutathione (GSH), and the activity of antioxidant enzymes. In the acute toxicity study, no adverse effects of OSWE were observed at doses up to 2000 mg/kg/day. Administration of OSWE reduced the damage by conditioning the gastric mucosa against ethanol-induced acute gastric injury, which included hemorrhage, hyperemia, and loss of epithelial cells. The level of MDA was reduced in OSWE-treated groups compared with the ethanol-induced group. Moreover, the level of GSH and the activity of antioxidant enzymes were significantly increased in the OSWE-treated groups. Our findings suggest that OSWE has a protective effect on the gastric mucosa against ethanol-induced acute gastric injury via the upregulation of antioxidant enzymes.
Highlights
It is well known that ethanol is metabolized mainly by alcohol dehydrogenases to form acetaldehyde, is further metabolized to form acetate, and has toxic effects on the gastrointestinal tract [1]
The EtOH group exhibited gastric mucosal injuries, including hemorrhage and hyperemia, the Ome group exhibited highly attenuated gastric mucosal injuries
These results demonstrated that Oryeongsan water extract (OSWE) has a protective effect that occurs via the reduction of hemorrhage, hyperemia, and loss of epithelial cells that are associated with gastric mucosal injury
Summary
It is well known that ethanol is metabolized mainly by alcohol dehydrogenases to form acetaldehyde, is further metabolized to form acetate, and has toxic effects on the gastrointestinal tract [1]. Intake of ethanol induces the overproduction of reactive oxygen species (ROS) and the decrease in the activity of antioxidant enzymes, such as catalase (CAT), glutathione S-transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD), and glutathione reductase (GR), leading to gastric mucosal injuries, including ulceration, erosion, hemorrhage, congestion, and edema [2, 3]. Gastric damage caused by ethanol increases oxidative stress, leading to the excessive production of ROS, which is the main cause of oxidative stress. Phenolic compounds can trap the free radicals directly or scavenge them through a series of coupled reactions with antioxidant enzymes. Many studies have demonstrated that antioxidant enzymes exhibit a protective effect on ethanol-induced gastric mucosal injury using various experimental animals [2, 6]. SpragueDawley rats have been used in virtually all disciplines of biomedical research including toxicology and pharmacology
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