Sulfonylurea is an oral hypoglycemic diabetes treatment drug. It lowers blood sugar levels by stimulating pancreatic β cells to secrete insulin. For type 2 diabetes, it can restore the peak of first-phase insulin secretion in response to glucose and increase first-phase insulin secretion. The insulin secretion response induced or stimulated by glucose after a meal is significantly increased. In addition, it may be involved in two mechanisms of diabetic complications by partially inhibiting platelet adhesion and aggregation and producing fibrinolytic activity on the vascular endothelium, reducing the process of microthrombosis.

1. Effect on water and electrolyte excretion: Increase the excretion of water, sodium, chloride, potassium, calcium, magnesium, phosphorus, etc., inhibit the active reabsorption of NaCl by the thick wall segment of the renal tubular loop, reduce the osmotic pressure gradient difference of the medullary interstitial fluid, resulting in increased excretion of water, Na+, and Cl-; promote the secretion of K+ by the distal tubule. 2. Effect on hemodynamics: Inhibit the activity of prostaglandin degrading enzymes, increase the content of prostaglandin E2, dilate blood vessels, increase renal blood flow; dilate pulmonary capacitance veins, reduce the permeability of pulmonary capillaries, reduce the amount of blood returning to the heart, and reduce the left ventricular end-diastolic pressure, which is helpful for the treatment of acute left heart failure.

It inhibits the synthesis of bacterial proteins through the bacterial transpeptidation process and has antibacterial effects on a variety of Gram-positive aerobic bacteria, Gram-negative aerobic bacteria, anaerobic bacteria, sexually transmitted disease microorganisms and other microorganisms.

It has a strong affinity for liver cholesterol metabolic enzymes, hinders the inactivation of cortisol and aldosterone, shows obvious corticosteroid-like effects (such as anti-inflammatory, anti-allergic and protective membrane structure), and has no obvious corticosteroid-like side effects; promotes bile pigment metabolism, reduces the release of ALT and AST; induces γ-IFN and interleukin II, increases NK cell activity and the OKT4/OKT8 ratio and activates the reticuloendothelial system; inhibits the release of histamine from mast cells; inhibits the formation of cell membrane phospholipase A2 (PL-A2) and prostaglandin E2 (PGE2) and granulomatous reactions; inhibits the production and formation of free radicals and lipid peroxides, and reduces the activity of prolyl hydroxylase; regulates calcium ion channels, and protects lysosomal membranes and mitochondria.

Monoammonium glycyrrhizinate has a strong affinity for liver cholesterol metabolism enzymes, thereby hindering the inactivation of cortisol and aldosterone. After use, it shows obvious corticosteroid-like effects, such as anti-inflammatory, anti-allergic and protective membrane structure, etc.; there are no obvious corticosteroid-like side effects. This product can promote bile pigment metabolism, reduce the release of ALT and AST; induce γ-IFN and interleukin II, increase NK cell activity and OKT4/OKT8 ratio and activate the reticuloendothelial system; inhibit mast cell release of histamine; inhibit the formation of cell membrane phospholipase A2 (PL-A2) and prostaglandin E2 (PGE2) and granulomatous reaction; inhibit the production and formation of free radicals and lipid peroxides, reduce the activity of proline hydroxylase; regulate calcium ion channels, protect lysosomal membranes and mitochondria, and reduce cell

Monoammonium glycyrrhizinate has a strong affinity for liver cholesterol metabolism enzymes, thereby hindering the inactivation of cortisol and aldosterone. After use, it shows obvious corticosteroid-like effects, such as anti-inflammatory, anti-allergic and protective membrane structure, etc.; there are no obvious corticosteroid-like side effects. This product can promote bile pigment metabolism, reduce the release of ALT and AST; induce γ-IFN and interleukin II, increase NK cell activity and OKT4/OKT8 ratio and activate the reticuloendothelial system; inhibit mast cell release of histamine; inhibit the formation of cell membrane phospholipase A2 (PL-A2) and prostaglandin E2 (PGE2) and granulomatous reaction; inhibit the production and formation of free radicals and lipid peroxides, reduce the activity of proline hydroxylase; regulate calcium ion channels, protect lysosomal membranes and mitochondria, and reduce cell

Monoammonium glycyrrhizinate has a strong affinity for liver cholesterol metabolism enzymes, thereby hindering the inactivation of cortisol and aldosterone. After use, it shows obvious corticosteroid-like effects, such as anti-inflammatory, anti-allergic and protective membrane structure, etc.; there are no obvious corticosteroid-like side effects. This product can promote bile pigment metabolism, reduce the release of ALT and AST; induce γ-IFN and interleukin II, increase NK cell activity and OKT4/OKT8 ratio and activate the reticuloendothelial system; inhibit mast cell release of histamine; inhibit the formation of cell membrane phospholipase A2 (PL-A2) and prostaglandin E2 (PGE2) and granulomatous reaction; inhibit the production and formation of free radicals and lipid peroxides, reduce the activity of proline hydroxylase; regulate calcium ion channels, protect lysosomal membranes and mitochondria, and reduce cell

This product belongs to the azole antifungal drugs. It has a wide antifungal spectrum. Oral and intravenous administration of this product is effective against fungal infections in humans and various animals, including Candida infection, Cryptococcus neoformans infection, Malassezia furfur, Microsporum, Trichophyton, Epidermophyton, Blastomyces dermatitidis, Coccidioides immitis, Histoplasma capsulatum, F. fischeri, Cladosporium carinii, etc. The mechanism of action of this product is mainly to highly selectively interfere with the activity of fungal cytochrome P-450, thereby inhibiting the biosynthesis of ergosterol on the fungal cell membrane.