It is a non-steroidal anti-inflammatory drug with analgesic, anti-inflammatory and antipyretic effects. This product exerts its pharmacological effects by inhibiting cyclooxygenase, reducing the synthesis of prostaglandins in local tissues, inhibiting the chemotaxis of leukocytes and the release of lysosomal enzymes.

Diclofenac 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 into prostaglandins. At the same time, it can also promote the combination of arachidonic acid with triglycerides (triacylglycerols), reduce the concentration of free arachidonic acid in cells, and indirectly inhibit the synthesis of leukotrienes. Diclofenac is a stronger non-steroidal anti-inflammatory drug, and its inhibitory effect on prostaglandin synthesis is stronger than that of aspirin and indomethacin.

This product has a broad-spectrum antimicrobial effect in vitro, 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 chloramphenicol. Chloramphenicol is fat-soluble, enters bacterial cells by diffusion, and reversibly binds to the 50S subunit of bacterial ribosomes, inhibiting the formation of peptide chains, thereby preventing protein synthesis.

This product has a broad-spectrum antimicrobial effect in vitro, 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 chloramphenicol. Chloramphenicol is fat-soluble, enters bacterial cells by diffusion, and reversibly binds to the 50S subunit of bacterial ribosomes, inhibiting the formation of peptide chains, thereby preventing protein synthesis.

It is a non-steroidal anti-inflammatory drug with analgesic, anti-inflammatory and antipyretic effects. This product exerts its pharmacological effects by inhibiting cyclooxygenase, reducing the synthesis of prostaglandins in local tissues, inhibiting the chemotaxis of leukocytes and the release of lysosomal enzymes.