The active substance of the drug Celeston is a fluorinated corticosteroid with long-acting betamethasone sodium phosphate. Its mineral corticoid activity is less pronounced due to the presence of the β-methyl group, which enhances the anti-inflammatory effect and reduces the property of fluoride to retain water and sodium.
Pharmacodynamics of this drug is based on the binding of the active substance to specific cell receptors and penetration into the cell nucleus, after which the synthesis of the lipocortin protein, which suppresses the anti-inflammatory activity of cyclogenases, phospholipase and other inflammatory factors, is increased. At the same time, the cytoplasmic membranes of inflammatory tissues are stabilized and the formation of antibodies is reduced.
Like all GCS, Celeston has an immunosuppressive effect, contributing to a decrease in the synthesis of T and B lymphocytes, a reduction in the production of lymphocytes and macrophages of γ-interferon and interleukins and a blockade of the output of the mediators of allergic reactions, in particular histamine, in the systemic circulation of the mast cells.
As a result of intracellular biochemical changes, the molecules of intercellular adhesion on membranes of endotheliocytes are neutralized and the movement of leukocytes to the site of inflammation stops, as well as the production of proteolytic enzymes and a tissue activator of plasminogen.
The use of Celeston in shock states not only restores receptor sensitivity to adrenaline, noradrenaline and dopamine, but also increases the level of catecholamines in the blood, stimulating the functions of the major organs and the overall metabolism.