Glucocorticosteroids for external use. Has a pronounced anti-inflammatory, antiallergic, antiexudative and antipruritic effect.
Interaction with intracellular glucocorticoid receptors - the formation of dimers of the glucocorticoid-glucocorticoid receptor complex. The steroid hormone complex with the receptor is transported to the nucleus of the cell. In the nucleus this complex interacts with effector elements localized on the acceptor sites of the chromatin (genes). As a result of the interaction, stimulation or inhibition of gene expression occurs; this leads to a change in the synthesis of matrix RNA and proteins.
The anti-inflammatory effect of flumethasone is due to several factors.
1. The drug induces the synthesis of lipocortin, which inhibits the activity of phospholipase A2. Inhibition of phospholipase-mediated A2 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 on the lipoxygenase pathway with the corresponding 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. Flumethasone 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.
With external application prevents the accumulation of neutrophils, which leads to a decrease in inflammatory exudate and production of lymphokines, inhibition of migration of macrophages, a reduction in infiltration and granulation.
Reduces the appearance or eliminates inflammatory skin reaction, softens burning and pain.