By blocking the membrane transport of calcium ions in myocardial and vascular smooth muscle, it inhibits the influx of calcium ions into cells, causing a decrease in myocardial contractility and vasodilation. Animal experiments have shown that by reducing myocardial contractility and peripheral vascular resistance, myocardial oxygen consumption is reduced; by dilating coronary vessels and developing collateral circulation, the oxygen supply to myocardial ischemic sites is increased; by inhibiting the consumption of high-energy phosphate compounds, the ability to resist hypoxia is enhanced.

Vitamin E is an antioxidant that can combine with selenium in the diet to prevent free radical damage to polyunsaturated fatty acids in membranes and other cell structures, protect red blood cells from hemolysis, protect nerves and muscles from oxygen free radical damage, maintain normal development and function of nerves and muscles, and may also be a cofactor for certain enzyme systems. Niacin is converted into nicotinamide in the body, and then combined with riboadenine to form nicotinamide adenine dinucleotide (coenzyme I) and nicotinamide adenine dinucleotide phosphate (coenzyme II), which are necessary for lipid, amino acid, protein, purine metabolism, tissue respiration oxidation and glycogenolysis. Niacin can reduce the utilization of coenzyme A and affect the transportation of cholesterol in the blood by inhibiting the synthesis of very low-density lipoprotein (VLDL).

This product is a gastrointestinal mucosal protective drug. After oral administration, it forms a sol with excellent colloidal properties in the gastric juice, which has a strong affinity with the ulcer surface and the inflamed surface, and can form an effective protective film to isolate gastric acid, protect the damaged mucosa, and stimulate the gastrointestinal mucosal epithelial cells to secrete mucus, promoting the self-repair of epithelial cells. This product has excellent adhesion to the damaged mucosa and has a hemostatic effect. This product can also kill gastric Helicobacter pylori. Animal experiments show that this product can reduce the number of ulcers in experimental ulcerative colitis rabbits, reduce the diameter of ulcers, and reduce the number of bowel movements and loose stools in experimental ulcerative colitis rabbits and rats.

After oral administration, it can form a protective film on the gastric mucosa and stimulate the gastric mucosal epithelial cells to secrete mucus, increasing the protective effect on the mucosa. In addition, it can kill Helicobacter pylori and promote the healing of gastritis.