Gastric mucin

Gastric mucin may be integrally involved in the mechanism of gastric mucosal injury caused by Helicobacter pylori leading to gastritis, peptic ulceration, and possibly gastric cancer^[1].
Gastric mucins are classified into two types based on their histochemical properties. The first is a surface mucous cell-type mucin, secreted from the surface mucous cells. The second is found in deeper portions of the mucosa and is secreted by gland mucous cells, including mucous neck cells, cardiac gland cells, and pyloric gland cells. The unique O-glycans in gastric mucin appears to function as a natural antibiotic, protecting the host from H. pylori infection^[2].
Gastric mucin may provide protection to the surface epithelium gastrointestinal tract by scavenging oxidants produced within the lumen; however, it does so at the expense of its viscoelastic properties. Both native and pronase-treated mucin effectively scavenge hydroxyl radical and that the scavenging properties are not significantly different. The effective concentration of mucin required for a 50% reduction in malondialdehyde production is 10 mg/mL for both native and pronase-treated mucin^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.