Acid and gastric mucosal protective drugs

The cause and mechanism of peptic ulcer are not completely clear. It is generally believed that the occurrence of peptic ulcer is the result of a combination of factors, mainly related to mucosal damage factors (gastric acid, pepsin), mucosal protective factors (stomach mucosa). Impairment of the barrier, mucosal blood circulation and epithelial renewal) is associated with Helicobacter pylori infection. It is generally believed that the occurrence of duodenal ulcer is related to the enhancement of mucosal injury factors, and the occurrence of gastric ulcer is often more closely related to the weakening of mucosal protective factors. There is gastric acid and pepsin in the gastric juice, and the self-digestion of the stomach leads to the formation of peptic ulcer. Gastric acid is secreted by gastric mucosal wall cells. There are three receptors on parietal cells, namely acetylcholine receptor, gastrin receptor and histamine (H2) receptor. Three receptors can stimulate the secretion of gastric acid due to the stimulation of the corresponding substances. Regardless of the substance stimulation, the secretion of gastric acid by parietal cells is controlled by the "H+-K+-ATP" enzyme, the "acid pump" (H+-K+ pump), which causes H+ to be secreted outside the parietal cells. When a variety of internal and external factors act to initiate the acid secretion mechanism of the stomach, resulting in excessive acid secretion, excessive gastric acid will cause damage to the gastric mucosa and form an ulcer. Pepsin is activated by the action of gastric acid or activated pepsin by pepsinogen secreted by the main cells of the gastric mucosa, and is another major damage factor of the gastric mucosa. In addition to digesting protein in food, pepsin can also hydrolyze glycoproteins and mucins in gastric mucus, destroying the mucous barrier of gastric mucosa and causing ulcer formation. The activity of pepsin is regulated by gastric acid. When the pH of gastric juice is between 1.8 and 2.5, the activity of pepsin is in an optimal state. The pH of gastric juice is increased and the activity of pepsin is weakened. The interaction of gastric acid and pepsin causes ulcer, and gastric enzyme plays a major role. The gastric and duodenal mucosa is covered by the mucus secreted by the epithelium. The mucus forms a line of defense with the intact epithelial cell membrane and the intercellular junction. It is called the mucus-mucosal barrier and protects the mucosa from digestion. Under normal circumstances, the thickness of mucus is about 10-20 times that of epithelial cells. The diffusion rate of H+ in mucus is relatively slow. In fact, the mucus layer provides a barrier for the mucosa to isolate the mucosa from the contents of the cavity and block it. H+ and pepsin damage to the mucosa. The proximal part of the stomach and duodenum can also secrete alkaline HCO3-, neutralize the gastric acid on the surface of the mucosa, so that the surface of the epithelial cells can maintain the pH range of 0-8, resist the dispersion of H+, and reduce the damage of gastric acid to the mucosa. In addition, the rich blood supply of the gastric mucosa and the continuous shedding of the epithelial cells can maintain the integrity of the gastric mucosa and block the reverse dispersion of H+. When the mucosal blood supply is insufficient and ischemic necrosis, the epithelial cells are renewed and regenerated, and ulcers may form. For example, neonatal asphyxia and hypoxia are prone to stress ulcers.