Uric acid is the final product of purine metabolism in the human body. Hyperuricemia is a group of diseases caused by decreased uric acid excretion or excessive uric acid production in the body. Uric acid is mostly excreted by the kidney, and hyperuricemia caused by poor renal excretion accounts for 90%. Renal insufficiency, decreased renal blood flow, decreased glomerular filtration rate and renal tubular excretion dysfunction can lead to decreased uric acid excretion; The easily invaded parts of urate crystals are the synovial membrane and articular cartilage of joints, kidney and subcutaneous soft tissue, resulting in gout, urinary acid nephropathy, urinary calculi or lesch2nyhan syndrome. In addition, hyperuricemia can also damage vascular endothelial cells, promote platelet aggregation, and induce cardiovascular diseases such as thrombosis and atherosclerosis.

    Clinically, allopurinol is used to inhibit the synthesis of uric acid, while probenecid and gout Lixian are used to promote the excretion of uric acid. Probenecid can inhibit the active reabsorption of uric acid in proximal convoluted renal tubules, increase the excretion of uric acid and reduce the concentration of uric acid in blood. It can be used in the treatment of chronic gout. However, probenecid has no anti-inflammatory and analgesic effects, and it often aggravates the symptoms in the early stage of gout, so it is not suitable for acute gout.   Scopolamine by intraperitoneal injection or intragastric administration could significantly inhibit hyperuricemia induced by potassium oxazinate and hypoxanthine in mice, increase the concentration of uric acid in urine, but had no significant effect on the activity of purine oxidase in liver. The results showed that scopolamine could reduce uric acid mainly by promoting uric acid excretion, but not by reducing uric acid synthesis in vivo. Moreover, the anti hyperuricemia drug prepared by scopolamine had no significant effect on the content of serum uric acid in normal mice; While promoting uric acid excretion, scopolamine has no diuretic effect, which indicates that scopolamine does not promote uric acid excretion through diuresis, but has the effect of promoting uric acid excretion by itself. It has the function of promoting uric acid excretion without diuretic effect. This single function makes it unnecessary for doctors to consider the influence of diuretic factors on patients when using the drug to treat hyperuricemia. In addition, scopolamine has a significant inhibitory effect on gouty arthritis induced by sodium urate crystallization in rats. The results showed that scopolamine could not only reduce the level of uric acid, but also inhibit the joint swelling caused by urate. It had the effect of treating gouty arthritis from both symptoms and signs, and its curative effect was better than that of allopurinol and probenecid.  

    In short,ScopolamineNo matter by injection or oral administration, it has significant curative effect and has no effect on normal serum uric acid. It can be used as a drug to prevent hyperuricemia. It has no diuretic effect while promoting uric acid excretion, especially in the treatment of gouty joint swelling.