Iron is a component of hemoglobin in red blood cells. When iron is deficient, the amount of hemoglobin synthesized by red blood cells decreases, causing the red blood cells to become smaller and their oxygen-carrying capacity to decrease, resulting in iron-deficiency anemia. Oral administration of this product can supplement iron and correct iron-deficiency anemia.

Participate in the body's antibody, collagen formation and tissue repair, as well as the metabolism of carbohydrates, fats and proteins, and maintain blood vessel integrity

Maintains normal vascular permeability and prevents capillary bleeding

It has a broad spectrum of antimicrobial effects, including aerobic Gram-negative and Gram-positive bacteria, anaerobes, Rickettsia, spirochetes and Chlamydia. It has bactericidal effects on Haemophilus influenzae, Streptococcus pneumoniae and Neisseria meningitidis; it only has antibacterial effects on anaerobic bacteria such as Staphylococcus aureus, Streptococcus pyogenes, Streptococcus viridans, Group B hemolytic Streptococcus, Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Salmonella typhi, Salmonella paratyphi, Shigella, Bacteroides fragilis, etc. Pseudomonas aeruginosa, Acinetobacter, Enterobacter, Serratia marcescens, indole-positive Proteus, methicillin-resistant Staphylococcus and Enterococcus are usually resistant to it. It inhibits protein synthesis by reversibly binding to the 50S subunit of the bacterial ribosome, and is completely cross-resistant with chloramphenicol. It has a strong immunosuppressive effect, which is about 6 times stronger than chloramphenicol.

Dihydropyridine calcium antagonists can selectively inhibit the transmembrane transport of calcium ions into myocardial cells and smooth muscle cells, and inhibit the release of calcium ions from intracellular pools without changing the plasma calcium ion concentration. It can simultaneously relax the coronary arteries in the normal blood supply area and the ischemic area, antagonize spontaneous or ergonovine-induced coronary artery spasm, increase the delivery of myocardial oxygen to patients with coronary artery spasm, and relieve and prevent coronary artery spasm. It can also inhibit myocardial contraction, reduce myocardial metabolism, and reduce myocardial oxygen consumption. On the other hand, it can relax peripheral resistance vessels, reduce peripheral resistance, reduce systolic and diastolic blood pressure, and reduce cardiac afterload. It can delay the sinoatrial node function and atrioventricular conduction of isolated hearts; electrophysiological studies on whole animals and humans have not found that this product has the effect of delaying atrioventricular conduction, prolonging the recovery time of the sinoatrial node, and slowing down the sinoatrial node rate.

Dihydropyridine calcium antagonists can selectively inhibit the transmembrane transport of calcium ions into myocardial cells and smooth muscle cells, and inhibit the release of calcium ions from intracellular pools without changing the plasma calcium ion concentration. It can simultaneously relax the coronary arteries in the normal blood supply area and the ischemic area, antagonize spontaneous or ergonovine-induced coronary artery spasm, increase the delivery of myocardial oxygen to patients with coronary artery spasm, and relieve and prevent coronary artery spasm. It can also inhibit myocardial contraction, reduce myocardial metabolism, and reduce myocardial oxygen consumption. On the other hand, it can relax peripheral resistance vessels, reduce peripheral resistance, reduce systolic and diastolic blood pressure, and reduce cardiac afterload. It can delay the sinoatrial node function and atrioventricular conduction of isolated hearts; electrophysiological studies on whole animals and humans have not found that this product has the effect of delaying atrioventricular conduction, prolonging the recovery time of the sinoatrial node, and slowing down the sinoatrial node rate.