This product is a second-generation sulfonylurea oral hypoglycemic drug. Its main mechanism of hypoglycemic effect is to stimulate pancreatic beta cells to secrete insulin and partially increase the sensitivity of surrounding tissues to insulin. This product binds to and dissociates from insulin receptors faster than glibenclamide and is less likely to cause severe hypoglycemia.

Vitamin D2 promotes the absorption of calcium by the brush border of the small intestinal mucosa and the reabsorption of phosphorus by the renal tubules, increases the concentration of blood calcium and phosphorus, cooperates with parathyroid hormone and calcitonin, promotes the release of calcium phosphate from old bones, and maintains and regulates the normal concentration of plasma calcium and phosphorus. Vitamin D2 promotes the deposition of calcium in new bone formation sites, deposits citrate in bones, promotes bone calcification and the maturation of osteoblast function and bone-like tissue. After vitamin D2 is ingested, it is catalyzed by the 25-hydroxylase system in the cell microsomes to produce calcidiol (25-OHD3), which is catalyzed by the 1-hydroxylase system of the renal proximal tubular cells to produce biologically active calcitriol [1-25-(OH)2D3].

Vitamin D2 promotes the absorption of calcium by the brush border of the small intestinal mucosa and the reabsorption of phosphorus by the renal tubules, increases the concentration of blood calcium and phosphorus, cooperates with parathyroid hormone and calcitonin, promotes the release of calcium phosphate from old bones, and maintains and regulates the normal concentration of plasma calcium and phosphorus. Vitamin D2 promotes the deposition of calcium in new bone formation sites, deposits citrate in bones, promotes bone calcification and the maturation of osteoblast function and bone-like tissue. After vitamin D2 is ingested, it is catalyzed by the 25-hydroxylase system in the cell microsomes to produce calcidiol (25-OHD3), which is catalyzed by the 1-hydroxylase system of the renal proximal tubular cells to produce biologically active calcitriol [1-25-(OH)2D3].

Epalrestat is a reversible non-competitive inhibitor of aldose reductase, which has a selective inhibitory effect on aldose reductase. Clinical studies have shown that epalrestat can inhibit the accumulation of sorbitol in erythrocytes of patients with diabetic peripheral neuropathy, and can improve the subjective symptoms and neurological dysfunction of patients compared with the control group. Animal experiments have shown that epalrestat can significantly inhibit the accumulation of sorbitol in the sciatic nerve, erythrocytes, and retina of diabetic model rats, and improve their motor nerve conduction velocity and autonomic nerve function; in terms of neuromorphology, epalrestat can improve axonal flow abnormalities, increase the density of myelinated nerve fibers in the sciatic nerve, the thickness of the myelin sheath of the sural nerve, the axon area, and the axon cylindrical rate; in addition, epalrestat can also improve the blood flow of the sciatic nerve of the model animal and restore its inositol content.

Extract from the above information