The development from hyperuricemia to gout: key mechanisms and natural products for treatment

Abstract

Gout is a common of inflammatory arthritis and is caused by the deposition of monosodium urate (MSU) crystals as a result of hyperuricemia (HUA). Although HUA is considered to be the main risk factor for gout, only approximately 10% of the individuals with HUA will eventually experience a gout attack. In this review, we first briefly introduce the development of gout and then summarize several possible reasons for its development. Genetic factors play a more prominent role in gout than in other diseases; functional mutations related to urate control and innate immunity components have been found to be associated with gout. Here, we list some of the most prominent genes involved in the pathogenesis of gout. In joints with MSU deposition, mature macrophages may uptake MSU crystals without causing inflammation, and this helps to maintain joints in an asymptomatic state. As an auxiliary inflammation pathway, the ATP-P2X7R-NLRP3 axis may contribute to the amplification of MSU-induced inflammation to affect the development of gout. Finally, this review summarizes the research progress on natural products that can be used in the treatment of HUA and gout.

Efficacy and Safety of Qinpi Tongfeng Formula in the Treatment of Acute Gouty Arthritis: A Double-Blind, Double-Dummy, Multicenter, Randomized Controlled Trial

“…e extract of Herba Siegesbeckiae can also inhibit the activity of xanthine oxidase and reduce serum uric acid [42]. Rhizome Dioscoreae Hypoglaucae has anti-inflammatory and analgesic effects Evidence-Based Complementary and Alternative Medicine [43,44]. e extract of Rhizome Dioscoreae Hypoglaucae can promote the excretion of uric acid by regulating the levels of organic anion transporter 1, murat1, and organic cation transporter 2 and has the effect of reducing uric acid [45].…”

A Selective Review and Virtual Screening Analysis of Natural Product Inhibitors of the NLRP3 Inflammasome

“…After, the active NLRP3 sensor oligomerizes and binds to the adaptor and effector parts of the inflammasome as mentioned earlier. Finally, this process leads to the release of active IL-1β from the cell, which causes an inflammatory effect and joint pain in gout patients [ 18 , 19 , 20 , 21 , 22 , 23 , 24 ].…”

Identification of Interleukin-1-Beta Inhibitors in Gouty Arthritis Using an Integrated Approach Based on Network Pharmacology, Molecular Docking, and Cell Experiments

“…When IL-1β is excessively produced, it can cause atherosclerosis, rheumatoid arthritis, gout, Parkinson's disease, Alzheimer's disease, tumors, and other diseases [12,13]. In particular, IL-1β plays a key role in the occurrence and development of GA [14].…”

“…When IL-1 β is excessively produced, it can cause atherosclerosis, rheumatoid arthritis, gout, Parkinson's disease, Alzheimer's disease, tumors, and other diseases [ 12 , 13 ]. In particular, IL-1 β plays a key role in the occurrence and development of GA [ 14 ]. Urate deposition in GA promotes the release of IL-1 β , which in turn promotes the influx of neutrophils into the joint to trigger joint inflammation [ 15 – 18 ].…”