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Abstract

Gouty arthritis, an inflammatory joint disease, occurs due to the accumulation of Monosodium Urate (MSU) crystals in the joints, mainly at the metatarsophalangeal joints of the big toe. At present, the incidence and prevalence of gout are increasing globally. The various risk factors are responsible for the development of gouty arthritis, including nonmodifiable, modifiable, and genetic factors. Under physiological conditions, the purine undergoes a catabolic pathway to produce the uric acid end product excreted from the body using various uric acid transporters. The overproduction or underexcretion of uric acid leads to the pathophysiology of hyperuricemia and promotes the MSU crystals formation and deposition in joints to trigger inflammation by releasing inflammatory mediators in gouty arthritis. If chronic gout has been left untreated, the pain worsens and eventually causes cartilage degradation, bone erosion, and urolithiasis. The research studies of the antigout activity of the various secondary metabolites are manifested in this review. The inflammatory pathways involved in gouty arthritis development are being discussed to find a new therapeutic target to treat gouty arthritis better. INTRODUCTION:In the 13 th century, Randolphus of bocking was the first person who coined the term "GOUT" which is derived from the Latin word "GUTTA" (which translates into "drop"). In the olden days the disease was believed to be caused by drops of viscous hum or (liquid) dripping from the blood into the joints, this explanation currently resembles the modern scientific explanation 1 . Gouty arthritis is a type of arthropathy in which joints are painful due to the accumulation of monosodium urate crystals. It usually affects the big toe (metatarsal joint). It can also affect other joints like the ankle, knee, foot,