Neomycin has a bactericidal effect, disrupting protein synthesis on the ribosomes of the bacterial cell and the permeability of the cytoplasmic membrane. Active in a relationship Staphylococcus aureus, Corynebacterium diphtheriae, Streptococcus viridans, Escherichia coli, Klebsiella pneumoniae, Proteus vulgaris, Aerobacter aerogenes, Haemophilus influenzae.
Dexamethasone has glucocorticoid, anti-allergic, anti-inflammatory, immunosuppressive and anti-shock effects.
Interaction with intracellular glucocorticoid receptors - the formation of dimers of the glucocorticoid-glucocorticoid receptor complex. Penetration of the activated receptor into the nucleus, binding to glucocorticoid-sensitive regulatory elements of DNA - a specific effect on gene expression (activation and inhibition).
The anti-inflammatory effect of dexamethasone is due to several factors.
1. The drug induces the synthesis of lipocortin, inhibiting the activity of phospholipase A2. Inhibition of phospholipase A mediated2 hydrolysis of membrane phospholipids of damaged tissues prevents the formation of arachidonic acid. The disruption of the formation of arachidonic acid actually means inhibition of the synthesis of prostaglandins, since arachidonic acid is a substrate for further metabolism along the cyclooxygenase pathway, and also along the lipoxygenase pathway, with appropriate inhibition of leukotriene synthesis.
2. The anti-inflammatory effect of glucocorticoids is potentiated by their ability to inhibit the expression of COX-2 genes, which also leads to a decrease in the synthesis of prostaglandins in the inflammatory focus, including pro-inflammatory prostaglandins E2 and I2.
3. Dexamethasone inhibits the expression of molecules of intercellular adhesion in the endothelium of blood vessels, violating the penetration of neutrophils and monocytes into the focus of inflammation. After the administration of glucocorticoids, an increase in the concentration of neutrophils in the blood (due to their entry from the bone marrow and the restriction of migration fromblood vessels). This causes a decrease in the number of neutrophils in the site of inflammation.
Glucocorticoids inhibit the transcription of cytokine genes that stimulate the inflammatory and immune response (IL-1, IL-2, IL-6, IL-8), as well as tumor necrosis factor (and some others). Also, a decrease in the transcription rate and an increase in the degradation of the receptor genes to IL-1 and IL-2, inhibition of transcription of the metalloproteinase (collagenase, elastase, etc.) genes involved in increasing the permeability of the vascular wall in the processes of scarring and destruction of the cartilaginous tissue in joint diseases are noted.
Immunosuppressive effect is due to inhibition of transcription of DNA encoding the main histocompatibility complex, pro-inflammatory cytokines and inhibition of proliferation of T-lymphocytes. It leads to a decrease in the number of T-lymphocytes and their influence on B-lymphocytes, inhibits the production of immunoglobulins. Reduces formation and increases the breakdown of the components of the compliment system.
The antiallergic effect is associated with inhibition of the synthesis of allergy mediators and inhibition of the release of mediators of allergy, and therefore it is effective in allergic reactions of immediate type.
When applied to the surface of the skin, the drug has a rapid and pronounced effect in the inflammatory focus, reducing the severity of objective symptoms (erythema, edema, lichenification) and subjective sensations (itching, irritation, pain).