Inhibits uric acid synthesis by inhibiting xanthine oxidase to prevent hypoxanthine and xanthine from being metabolized into uric acid, thereby reducing uric acid production, lowering the uric acid content in the blood and urine, and preventing the deposition of uric acid crystals. It helps to redissolve uric acid crystals in the tissues of gout patients, while inhibiting the synthesis of new purines in the body.

Antipyretic, anti-inflammatory, analgesic, sedative, anticonvulsant

Inhibits a variety of pathogenic microorganisms

Niuhuang Jiedu Tablets have obvious antipyretic, anti-inflammatory, analgesic, sedative and anticonvulsant effects, and have a strong inhibitory effect on a variety of pathogenic microorganisms that cause various inflammations.

Niuhuang Jiedu Tablets have obvious antipyretic, anti-inflammatory, analgesic, sedative and anticonvulsant effects, and have a strong inhibitory effect on a variety of pathogenic microorganisms that cause various inflammations.

Niuhuang Jiedu Tablets have obvious antipyretic, anti-inflammatory, analgesic, sedative and anticonvulsant effects, and have a strong inhibitory effect on a variety of pathogenic microorganisms that cause various inflammations.

Niuhuang Jiedu Tablets have obvious antipyretic, anti-inflammatory, analgesic, sedative and anticonvulsant effects, and have a strong inhibitory effect on a variety of pathogenic microorganisms that cause various inflammations.

Niuhuang Jiedu Tablets have obvious antipyretic, anti-inflammatory, analgesic, sedative and anticonvulsant effects, and have a strong inhibitory effect on a variety of pathogenic microorganisms that cause various inflammations.

Niuhuang Jiedu Tablets have obvious antipyretic, anti-inflammatory, analgesic, sedative and anticonvulsant effects, and have a strong inhibitory effect on a variety of pathogenic microorganisms that cause various inflammations.

It combines with blood ammonia in the body to form urea and is excreted from the body, which has the effect of reducing blood ammonia and promoting brain metabolism. It may be a central mediator that can enhance the activity of glucose phosphatase and facilitate the recovery of brain cell function.

Aldosterone antagonist. It can inhibit the sodium retention, potassium excretion and water retention caused by the action of aldosterone on the distal renal tubule. When the blood aldosterone concentration is not high, the effect of this product is also weak. On the contrary, when secondary aldosterone increases, the effect of this drug is significant.

Calcium ions are necessary to maintain the normal functions of nerves, muscles and bones; they can promote the calcification of bones and teeth. They also play an important role in maintaining normal heart, kidney, lung and coagulation functions, as well as cell and capillary permeability. In addition, calcium is also involved in regulating the secretion and storage of neurotransmitters and hormones, maintaining the normal excitability of nerves and muscles, as well as the intake and binding of amino acids and the absorption of vitamin B12.

It forms thiamine pyrophosphate in the body and is a necessary coenzyme for carbohydrate metabolism, which can maintain the normal functions of the heart, nerves and digestive system. Vitamin B1 can inhibit the activity of cholinesterase. When it is deficient, the activity of cholinesterase is enhanced, the hydrolysis of acetylcholine is accelerated, and the conduction of nerve impulses is impaired, affecting the gastrointestinal and myocardial functions.

It 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 to promote the release of calcium phosphate from old bones, and maintains and regulates the normal concentration of plasma calcium and phosphorus. It promotes the deposition of calcium in the new bone formation site, deposits citrate in the bone, 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 microsomes of liver cells 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].