In gout, inflammation in joints results from the precipitation of circulating uric acid, exceeding its solubility in blood and depositing as crystals of monosodium urate in and around synovial fluid and soft tissues of joints. These crystal deposits cause inflammatory arthritis, which is initiated and sustained by mechanisms involving various proinflammatory mediators, such as cytokines.<unk>  accumulates in white blood cells and affects them in a variety of ways - decreasing motility, mobilization (especially chemotaxis), and adhesion. Under preliminary research are various mechanisms by which<unk>  may interfere with gout inflammation: *Inhibits microtubule polymerization by binding to its constitutive protein, tubulin *As availability of tubulin is essential to mitosis,<unk>  may inhibit mitosis *Inhibits activation and migration of neutrophils to sites of inflammation *Interferes with the inflammasome complex found in neutrophils and monocytes that mediate interleukin-1β activation, a component of inflammation *Inhibits superoxide anion production in response to urate crystals *Interrupts mast cell and lysosome degranulation *Inhibits release of glycoproteins that promote chemotaxis from synovial cells and neutrophils Generally,<unk>  appears to inhibit multiple proinflammatory mechanisms, while enabling increased levels of anti-inflammatory mediators. Apart from inhibiting mitosis,<unk>  inhibits neutrophil motility and activity, leading to a net anti-inflammatory effect, which has efficacy for inhibiting or preventing gout inflammation.
Colchicine
Diclofenac
Ketoprofen
Aceclofenac
Meclofenamic acid
Allopurinol
Diclofenamide
Indoprofen