Prednisolone (Prednisolon )

Prednisolone is a synthetic glucocorticoid drug, a dehydrated analog of hydrocortisone. Has anti-inflammatory, antiallergic, desensitizing, anti-shock, antitoxic and immunosuppressive action.

Interacts with specific cytoplasmic receptors and forms a complex penetrating into the nucleus of the cell, stimulates the synthesis of matrix ribonucleic acid (mRNA); the latter induces the formation of proteins, incl. lipocortin, mediating cellular effects. Lipocortin depresses phospholipase A2, inhibits the release of arachidonic acid and inhibits the synthesis of endoperoxides, prostaglandins, leukotrienes, which promote inflammation, allergies, etc.

Suppresses the release of the adrenocorticotropic hormone by the pituitary gland and, secondarily, the synthesis of endogenous glucocorticosteroids. Inhibits the secretion of thyroid-stimulating and follicle-stimulating hormones.

Reduces the number of lymphocytes and eosinophils increases - erythrocytes (stimulates the production of erythropoietins).

Protein metabolism: reduces the amount of protein in the plasma (due to globulins) with increasingcoefficient albumin / globulin, increases the synthesis of albumins in the liver and kidneys: enhances protein catabolism in muscle tissue.

Lipid metabolism: increases the synthesis of higher fatty acids and triglycerides, redistributes fat (accumulation of fat mainly in the area of ​​the shoulder girdle, face, abdomen), leads to the development of hypercholesterolemia.

Carbohydrate metabolism: increases the absorption of carbohydrates from the gastrointestinal tract; increases the activity of glucose-6-phosphatase, leading to an increase in the intake of glucose from the liver into the blood; increases the activity of phosphoenolpyruvate carboxylase and the synthesis of aminotransferases leading to the activation of gluconeogenesis.

Water-electrolyte exchange: retards sodium and water in the body, stimulates the excretion of potassium (mineralocorticoid activity), reduces the absorption of calcium from the gastrointestinal tract, "flushes" calcium from the bones, increases its excretion by the kidneys.

Anti-inflammatory effect is associated with inhibition of the release of eosinophils and mast cells by inflammatory mediators, inducing lipocortin formation and reducing the number of mast cells that produce hyaluronic acid; with a decrease in capillary permeability, stabilization of cell membranes and membranes of organelles (especially lysosomal ones).

Antiallergic effect develops as a result of suppression of synthesis and secretion of mediators of allergy, inhibition of release from sensitized mast cells and basophils of histamine and other biologically active substances, a decrease in the number of circulating basophils, suppression of lymphoid and connective tissue development, and a decrease in the number of T and B lymphocytes. mast cells, reducing the sensitivity of effector cells to mediators of allergy, inhibition of antibody formation. changes in the immune response of the body.

In obstructive airway diseases the action is mainly based on the inhibition of inflammatory processes, the inhibition of development or prevention of edema of the mucous membranes, inhibition of eosinophilic infiltration of the submucosal layer of bronchial epithelium, and the deposition of circulating immune complexes in the mucosa of the bronchi. There is inhibition of erosion and desquamation of the mucous membrane. Prednisolone increases the sensitivity of beta-adrenergic receptors of bronchi of small and medium caliber to endogenous catecholamines and exogenous sympathomimetics, reduces the viscosity of mucus due to oppression or reduction of its production.

Anti-shock and antitoxic action is associated with an increase in blood pressure (by increasing the concentration of circulating catecholamines and restoring the sensitivity of adrenoreceptors to them, as well as vasoconstriction), a decrease in the permeability of the vascular wall, membrane-protective properties, activation of liver enzymes involved in the metabolism of endo- and xenobiotics.

Immunodepressive effect is caused by oppression of lymphocyte proliferation (especially T-lymphocytes), suppression of B-cell migration, and interaction of T and B lymphocytes. inhibition of the release of cytokines (interleukin-1, interleukin-2, gamma-interferon) from lymphocytes and macrophages and a decrease in the formation of antibodies.

It inhibits connective tissue reactions during the inflammatory process and reduces the possibility of scar tissue formation.