Suzhou Pharmaceutical Factory

Unspecified

This product belongs to the aminoglycoside antibiotics. The antibacterial spectrum is similar to that of gentamicin. It has antibacterial effects on Gram-negative bacteria such as Escherichia coli, aerogenes, Klebsiella, Proteus mirabilis, some indole-positive Proteus, Pseudomonas aeruginosa, some Neisseria, some non-pigmented Serratia and Shigella; the antibacterial effect of this product on Pseudomonas aeruginosa is 3 to 5 times stronger than that of gentamicin, and Pseudomonas aeruginosa that is moderately sensitive to gentamicin is highly sensitive to this product. Among Gram-positive bacteria, Staphylococcus aureus (including β-lactamase-producing strains) is sensitive to this product; Streptococci (including Streptococcus pyogenes, Pneumococcus, Streptococcus faecalis, etc.) are all resistant to this product. Anaerobic bacteria (Bacteroides), Mycobacterium tuberculosis, Rickettsia, viruses and fungi are also resistant to this product. The mechanism of action of this product is to bind to the 30S subunit of the bacterial ribosome and inhibit the synthesis of bacterial proteins.

Extract from the above information

This product is a proton pump inhibitor of gastric parietal cells. It can specifically inhibit the secretory microtubules and tubular vesicles in the cytoplasm of the parietal cell apical membrane, thereby effectively inhibiting the secretion of gastric acid. Since H, K-ATPase is the last process of acid secretion of parietal cells, this product has a strong acid inhibition ability. It can not only non-competitively inhibit gastric acid secretion caused by gastrin, histamine, choline and food stimulation of the vagus nerve, but also inhibit part of the basic gastric acid secretion that is not affected by choline or H2 receptor blockers. It also has a strong and lasting inhibitory effect on gastric acid secretion caused by dibutyl cyclic adenosine monophosphate (DCAMP) stimulation that cannot be inhibited by H2 antagonists. This product also has an inhibitory effect on pepsin secretion and changes in gastric mucosal blood flow.

Azithromycin is an azalide antibiotic, and its mechanism of action is to interfere with the synthesis of proteins (without affecting the synthesis of nucleic acids) by binding to the subunits of the 50s ribosomes of sensitive microorganisms. In vitro tests and clinical studies have shown that azithromycin is effective against the following pathogens: Gram-positive aerobic microorganisms: Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, and hemolytic streptococci. Azithromycin has cross-resistance to erythromycin-resistant Gram-positive bacteria. Most fecal streptococci (enterococci) and methicillin-resistant Staphylococci are resistant to this product. Gram-negative aerobic microorganisms: Haemophilus influenzae, Moraxella catarrhalis, and Mycoplasma trachomatis. In vitro tests and clinical studies have confirmed that this product can prevent diseases caused by the avian intracellular mycobacterium complex (composed of avian intracellular mycobacterium and intracellular mycobacterium). This product is ineffective against strains that produce beta-lactamase. In vitro research results have been obtained for the following microorganisms, but their clinical significance is still unclear, including Streptococcus (C, F, G), viridans streptococci, Bordetella pertussis, Haemophilus dukei, Legionella pneumophila, Bacteroides, Peptostreptococcus, Borrelia burgdorferi, Chlamydia pneumoniae, Treponema pallidum, Ureaplasma urealyticum, etc.