Protective Effect of Oat Polysaccharides against Acute Gastric Mucosal Injury in Mice

The present study aimed to investigate the protective effect of oat polysaccharides on 70% ethanolinduced acute gastric mucosal injury in mice.

Sixty Kunming male mice were randomly divided into normal, model, cimetidine (positive control), and low-, medium- and high-dose oat polysaccharide groups. The positive control group was gavaged with 100 mg/kg m_b of cimetidine, and the low-, medium- and high-dose oat polysaccharide groups were intragastrically administered with 100, 200, 400 mg/kg m_b of oat polysaccharides, respectively. The administration lasted for 14 consecutive days. On the 15^th day, acute gastric mucosal injury was successfully by oral administration of 70% ethanol to all animals except those in the normal group. Afterwards, visceral organ indexes and the degree of gastric mucosal injury were examined and gastric pH, serum nitric oxide (NO) levels, and the levels of interleukin (IL)-10, lipopolysaccharide (LPS), vascular endothelial growth factor (VEGF), malondialdehyde (MDA), glutathione (GSH), pepsin activity and superoxide dismutase (SOD) activity in gastric tissues were measured.

Compared with the model group, gastric mucosal injury in the mice treated with oat polysaccharides was significantly reduced, and the most pronounced effect was observed at the high-dose level with an inhibition rate of 76.04%. Furthermore, oat polysaccharides increased the pH of gastric juice, serum NO levels, the activity of SOD and the contents of GSH and VEGF in gastric tissue, and reduced the activity of pepsin and the content of LPS in gastric tissue, especially at the high dose.

Oat polysaccharides significantly protect against ethanol-induced acute gastric mucosal injury in mice with the most pronounced effect being observed at the high dose. The mechanism may be related to the increase in the pH of gastric juice, serum NO levels and the content of VEGF in gastric tissue, the decrease in LPS content and pepsin activity, and the enhancement of antioxidant capacity in the gastric mucosa.