Indications for use of CARSIL FORTE (Silymarin) are:

Toxic liver damage (alcoholism, intoxication with halogenated hydrocarbons, heavy metal compounds, medicinal liver damage), chronic hepatitis, liver cirrhosis (as part of complex therapy), lipid metabolism disorders.

Pharmacodynamics:

Karsil® Forte contains milk thistle fruit extract, the main active ingredients of which are a mixture of 6 isomers of flavonolignans (silymarin): silibinin A and B, isosilybinin A and B, silidianin and silicristin. Of these, silibinin is the most active. The mechanism of hepatoprotective action is not fully understood, the existing data prove the presence of several main mechanisms of action

Antioxidant action. Silymarin interacts with free radicals in the liver and converts them into less toxic compounds, interrupting the process of lipid peroxidation, prevents the destruction of cellular structures by binding to free radicals and regulating the intracellular content of glutathione. Depending on the concentration, it inhibits microsomal peroxidation caused by NADPH-Fe2 + -ADP. Influences enzyme systems associated with glutathione and superoxide dismutase. The components of silymarin inhibit the peroxidation of linolenic acid, catalyzed by lipoxygenase, and protect hepatic mitochondria and microsomes from the formation of lipid peroxides caused by various agents.

Membrane stabilizing action. Silymarin stabilizes cell membranes and regulates their permeability, thereby preventing the entry of hepatotoxic agents into hepatocytes. It has been established that the membrane-stabilizing effect of silymarin is due to its competitive interaction with receptors for the corresponding toxins on the hepatocyte membrane. The effect of silymarin on membrane permeability is associated with qualitative and quantitative changes in membrane lipids - cholesterol and phospholipids.

Silymarin stimulates regeneration processes in the liver (restoration of damaged hepatocytes) as a result of activation of the synthesis of structural and functional proteins (ribosomal synthesis of RNA, protein and DNA) and phospholipids. It has been experimentally established that silymarin also inhibits the transformation of stellate liver cells into myofibroblasts, a process responsible for the arrangement of collagen fibers.

Anti-inflammatory action. Experimental studies have shown that silybin at a certain concentration can inhibit the synthesis of LT B4 (leukotriene B4 / LTB4) in isolated Kupffer cells of animals. Silymarin, silybin, silidianin and silicristin inhibit the activity of lipoxygenase and prostaglandin synthase in vitro. In vitro studies on human polymorphonuclear leukocytes have shown that one of the mechanisms of the anti-inflammatory effect of silybin is the suppression of the formation of hydrogen peroxide.

Clinically, the pharmacodynamic properties of silymarin are expressed in the improvement of subjective and objective symptoms and the normalization of indicators of the functional state of the liver (transaminase, gamma globulin, bilirubin).

Pharmacokinetics:

Suction. After oral administration, silymarin is not completely absorbed from the gastrointestinal tract (up to 23–47%). Plasma Cmax is reached within 4-6 hours after oral administration of a single dose.

Distribution. In studies with 14C-labeled silibinin, the highest concentrations are found in the liver, lungs, stomach and pancreas, and in small quantities in the kidneys, heart and other organs.

Metabolism. Undergoes enterohepatic recirculation. It is metabolized in the liver by conjugation with sulfates and glucuronic acid. Glucuronides and sulfates were found as metabolites in bile.

Excretion. T1 / 2 is 1–3 hours for unchanged silymarin and 6–8 hours for its metabolites. It is excreted mainly in the bile (about 80%) in the form of glucuronides and sulfates, to a small extent (about 5%) by the kidneys in an unchanged form. Does not cumulate.