Jinyao Yongguang (Hebei) Pharmaceutical Co., Ltd.

Stabilize mast cell membranes, stop mast cells from releasing allergenic mediators such as histamine, leukotrienes, 5-hydroxytryptamine, bradykinin and slow-reacting substances, thereby preventing the occurrence of allergic reactions

This product is a broad-spectrum antibiotic, the mechanism of action is to inhibit bacterial protein synthesis, and is effective against most Gram-negative and some Gram-positive bacteria, as well as Chlamydia trachomatis and Rickettsia.

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 with triglycerides, reduce the concentration of free arachidonic acid in cells, and indirectly inhibit the synthesis of leukotrienes. Animal experiments have confirmed that prostaglandins are one of the mediators of intraocular inflammation, which can lead to the collapse of the blood-aqueous barrier, vasodilation, increased vascular permeability, leukocyte chemotaxis, non-cholinergic mechanism pupil constriction, etc. Diclofenac sodium is a stronger non-steroidal anti-inflammatory drug. Its inhibitory effect on prostaglandin synthesis is stronger than that of aspirin and indomethacin. Diclofenac sodium eye drops have a significant protective effect on the destruction of the blood-aqueous barrier caused by mechanical, chemical, biological and other stimuli.

It has special effects on Staphylococcus (Staphylococcus aureus, Staphylococcus epidermidis and penicillin-resistant strains), Streptococcus (Group A hemolytic streptococci, non-hemolytic streptococci and Streptococcus pneumoniae), Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae, Escherichia coli, Proteus mirabilis (indole-negative and indole-positive), Haemophilus influenzae and Haemophilus conjunctivitis, Moraxella conjunctivitis, Acinetobacter calcoaceticus (Herellea vaginacola), and Neisseria. It is still sensitive to gentamicin-resistant strains, and long-term use may lead to bacterial resistance.

This product is a nucleoside antiviral drug that has a selective inhibitory effect on a variety of herpes viruses (HSV). After acyclovir enters HSV-infected cells, it binds to the specific thymidylate kinase encoded by the virus and is rapidly converted into acyclosine monophosphate, which is then converted into acyclosine diphosphate by the cell's guanylate kinase. It is then converted into acyclosine triphosphate by other cell enzymes, and competes with guanylate triphosphate to infect herpes simplex virus DNA polymerase, thereby inhibiting viral DNA synthesis. Acyclovir triphosphate is a very strong viral DNA polymerase inhibitor, and has an inhibitory effect on the DNA polymerases of five human herpes viruses, namely HSV-1, HSV-2, VZV, CMZ and EBV. It has no effect on normal cells, and its antiviral efficacy is 160 times stronger than that of adenosine.