Glutoxim®
Glutoxim® has an immunomodulatory, hemostimulating, detoxifying, hepatoprotective effect, suppresses the drug resistance of tumor cells to anthracycline antibiotics, alkylating agents; helps overcome drug resistance of Mycobacterium tuberculosis
to isoniazid, associated with the katG (catalase-peroxidase gene) and inhA (enol-ACP reductase gene) genes.
Glutoxim® potentiates the effect of doxorubicin on tumor cells, chemotherapy agents (isoniazid, rifampicin, rifabutin, cycloserine, capreomycin, levofloxacin, cationic antimicrobial peptide catalecidin) on Mycobacterium tuberculosis
.
The immunomodulatory effect of the drug Glutoxim® is due to a receptor-mediated effect on calcium-dependent signaling pathways of macrophages, which leads to an increase in:
— survival and functional capacity of tissue macrophages;
— exocytosis of submembrane granules with intracellular parasitic forms of Mycobacterium tuberculosis
;
— activity of lysosomal enzymes;
— formation of reactive oxygen species;
— absorption and death of microorganisms;
- secretion of cytokines: interleukin 1, interleukin 6, tumor necrosis factor, interferons, erythropoietin, interleukin 2; cationic antimicrobial peptides - defensins, catalecidins.
The hemostimulating effect of the drug Glutoxim® is due to a receptor-mediated increase in bone marrow hematopoiesis: the processes of erythropoiesis, lymphopoiesis and granulocytomonocytopoiesis. The effect on progenitor cells of different lines of blood cells is mediated by the functioning of the MAP and inositol kinase systems, leads to an increase in the stability of differentiating hematopoietic cells, and restores their sensitivity to the action of endogenous hematopoietic factors.
The detoxifying and hepatoprotective effects of the drug are due to a receptor-mediated increase in the expression of enzymes of the second phase of detoxification of xenobiotics, including glutathione reductase, glutathione peroxidases, glutathione-S-transferase, glucose-6-phosphate dehydrogenase, heme oxygenase-1, an increase in the intracellular level of reduced glutathione, providing protection to cellular structures from the toxic effects of radicals.
Glutoxim® has a direct inhibitory effect on the activity of the multidrug resistance factor of tumor cells - the protein P-glycoprotein (Pgp), which determines the resistance of tumor cells to the action of chemotherapy, including anthracycline antibiotics and alkylating drugs.
Glutoxim® initiates the transformation reaction of isoniazid, a prodrug, into a pharmacologically active form, isonicotinic acid, which has a bacteriostatic effect on Mycobacterium tuberculosis
, which makes it possible to overcome drug resistance
of Mycobacterium tuberculosis
caused by negative transformation of the katG (catalase-peroxidase gene) and inhA (enol-ACP reductase gene) genes.
Glutoxim® stimulates the processes of exocytosis of vesicles from macrophages with intracellular parasitic microorganisms, including Mycobacterium tuberculosis
, ensuring their removal from the pharmacological refuge and making them available for the action of antibacterial drugs, including isoniazid, rifampicin, rifabutin, cycloserine, capreomycin, levofloxacin.
Glutoxim® enhances the secretion of cationic peptides - defensins and catalecidins by macrophages, stimulates their absorption by Mycobacterium tuberculosis, determining the indirect antibacterial effect of the drug.
When does psoriasis start?
It is difficult to pinpoint exactly when the disease began. Typically, a patient consults a doctor if he already has grounds for complaints. However, in 75% of cases, psoriasis affects people during puberty - the time of puberty. According to German experts, psoriasis is divided into two types: the first appears at the age of about 20 years and is somewhat more severe, the second occurs around 50 years. There is a possibility that psoriasis will begin in youth if one of your relatives has already been diagnosed with it. But, unlike other hereditary diseases, the nature of the transmission of psoriasis from generation to generation is not obvious, therefore it is impossible to predict with certainty whether any family members will get sick and who exactly.
So you can become a victim of psoriasis at any time, from infancy to old age.
Dermatology
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Genetic predisposition to psoriasis
Hereditary factors play a significant role in the development of this disease - this is indicated by the fact that it is more common in people whose relatives already suffer from psoriasis. The risk of developing psoriasis in a child whose parents are healthy is 12%. When psoriasis is diagnosed in the father or mother, the probability increases - this is already 10-20%. If both parents are sick, the risk for the child will be as much as 50%.
Scientists now believe that the inheritance of psoriasis is multifactorial, that is, several different genes are responsible for the predisposition to this disease, and in order for it to develop, several different external or internal factors are needed. Let's look at which ones exactly.
