No specific description provided

Dirithromycin is a macrolide antibiotic that inhibits protein synthesis by binding to the 50S ribosomal subunit of sensitive microorganisms. It is active against aerobic Gram-positive microorganisms (such as Staphylococcus aureus, Streptococcus pneumoniae, Streptococcus pyogenes), aerobic Gram-negative microorganisms (such as Haemophilus influenzae, Legionella pneumophila, Moraxella catarrhalis) and other microorganisms (such as Mycoplasma pneumoniae). In vitro tests have shown that it is also active against Listeria monocytogenes, Staphylococcus (C.F.G group), Bordetella pertussis, Propionibacterium acnes, etc., but the clinical significance is not yet fully understood. Bacteria resistant to other macrolide antibiotics are also resistant to this product.

It has astringent, gastric mucosal protective and antibacterial effects. After oral administration, a protective film is formed on the gastric mucosal wound surface, reducing the irritation of food to the gastric mucosa; in the intestine, bismuth combines with hydrogen sulfide to form insoluble bismuth sulfide (Bi2S3) on the intestinal mucosa, slowing down intestinal peristalsis; at the same time, bismuth salts also have antibacterial effects.

Because the thiol group in its chemical structure can break the disulfide bonds of mucin, it can reduce the viscosity of sputum and make it easier to cough up sputum.

Because the thiol group in its chemical structure can break the disulfide bonds of mucin, it can reduce the viscosity of sputum and make it easier to cough up sputum.

Because the thiol group in its chemical structure can break the disulfide bonds of mucin, it can reduce the viscosity of sputum and make it easier to cough up sputum.

Because the thiol group in its chemical structure can break the disulfide bonds of mucin, it can reduce the viscosity of sputum and make it easier to cough up sputum.

Diclofenac sodium is a non-steroidal anti-inflammatory analgesic derived from phenylacetic acid. Its mechanism of action is to inhibit the activity of cyclooxygenase, thereby blocking the conversion of arachidonic acid to prostaglandins. At the same time, it can also promote the combination of arachidonic acid and triglycerides, reduce the concentration of free arachidonic acid in cells, and indirectly inhibit the synthesis of leukotrienes. Diclofenac sodium is a stronger non-steroidal anti-inflammatory drug. Its inhibitory effect on prostaglandin synthesis is stronger than that of aspirin and indomethacin.