I. General treatment: Try to remove factors that cause bile reflux, such as alcohol consumption, smoking, and irritating foods and drinks. Maintain an optimistic mood, develop good dietary and hygienic habits, advocate the consumption of vegetables, green tea and foods rich in folic acid and carotene. Some studies have found that long-term supplementation with antioxidants, vitamins, folic acid and carotene has a certain effect on preventing and blocking gastric mucosal atrophy. Second, the application of gastric mucosal protective agents In response to the role of bile reflux on gastric mucosal damage, in recent years, people began to pay attention to gastric mucosal protection remember to apply, such as: 1, prostaglandin E: a protective effect on gastric mucosal cells, can stimulate the secretion of mucus and HCO3-, dilate blood vessels, promote the blood circulation of the mucosa, inhibit the secretion of gastric acid and pepsin, increase exogenous PGE1. 2, teprenone: a terpene, can promote the biosynthesis of glycolipid intermediates in gastric mucosal microsomes, and then accelerate the synthesis of the main mucosal repair factor, i.e. polymeric glycoprotein, in gastric mucosa and gastric mucus layer, and increase the concentration of phospholipids in mucus, thus improving the defense function of mucosa. 3. Sixteen-angle montmorillonite (Simethicone): It mainly strengthens the role of gastric mucosal barrier, fixes the role of inhibiting and eliminating viruses and germs, adsorbs gas in the digestive tract and resists various attack factors. Third, reduce bile absorption and improve gastric motility 1, drugs to reduce bile absorption (1) koelenamine (biliary amine): can form chelates with bile acids in the intestine and excrete with feces, the amount of bile acids excreted is 3 to 4 times more than normal. It can complex the bile salts that reflux into the stomach and prevent bile acids from destroying the gastric mucosal barrier. (2) Aluminum thioglycollate: It can complex with pepsin to inhibit the activity of this enzyme, and can complex with mucin of gastric mucosa to form a protective film, and can also bind with bile acid and lysolecithin. (3) Ursodeoxycholic acid (UDCA): It has good biliary effect and can relax the biliary sphincter and play the role of bile excretion. The most toxic effect of bile on gastric mucosa is deoxycholic acid and stone bile acid. In the gastric juice of patients with bile reflux, bile acids are mainly bile acids and deoxycholic acid, and UDCA only accounts for 1%. Taking UDCA, bile acid in gastric juice to UDCA mainly, and bile acid, deoxycholic acid and stone bile acid concentration decreased significantly, thus reducing the latter two damage to the gastric mucosa. (4) magnesium aluminum carbonate: is a new type of bile acid binding drugs, containing a special laminar network structure, can adsorb and bind pepsin, bile acid, lysolecithin, etc., thus weakening the attack of mucosal damage factors. It promotes mucus secretion, synthesis and release of protective prostaglandins such as PGI from gastric mucosal cells, promotes mucosal blood flow, and can neutralize gastric acid rapidly. On the other hand, it binds bicarbonate and converts into bicarbonate reservoir, similar to physiological gastric mucosal barrier protection mechanism. Combining with bile acid in acidic environment clears the damage of bile acid to gastric mucosa, and can release bile acid in alkaline environment in intestine, never affecting the hepatic and intestinal circulation of bile acid. 2, drugs that promote gastrointestinal motility such as metoclopramide (gastrofluan), domperidone (morpholine), cisapride tablets, mosapride, and six flavors of antifluan can enhance the contraction of the gastric body and sinus section, increase the tension of the stomach, improve the coordination of the sinus section and duodenum, accelerate gastric emptying, prevent and control bile reflux, regulate and restore gastrointestinal motility.