Hypouricemic Effect of Ethanol Extract of Aster glehni Leaves in Potassium Oxonate-Induced Hyperuricemic Rats

Abstract

The prevalence of gout is increasing worldwide, and control of serum uric acid level has been regarded as one of the therapeutic methods for gout. Inhibition of xanthine oxidase (XO) activity which can oxidize hypoxanthine to uric acid has been commonly proposed to decrease serum uric acid level. The aim of this study was to demonstrate the hypouricemic effect of ethanol extract of Aster glehni leaves (EAG) by in vitro and in vivo study in potassium oxonate (PO)-induced hyperuricemic rats. EAG possessed 132.5 ± 6.8 mg QE/g of total flavonoid and showed antioxidant activity. EAG showed in vitro and in vivo inhibitory activity against XO and significantly decreased serum uric acid level in PO-induced hyperuricemic rats without liver toxicity. These results show that EAG significantly attenuates hyperuricemia by inhibiting XO activity, which resulted in the decrease of serum uric acid level. Therefore, EAG might possess a potential therapeutic ability for improving gout.

Evaluation of the anti-gout effect of Sonchus Arvensis on monosodium urate crystal-induced gout arthritis via anti-inflammatory action - an in vivo study

“…The underlying mechanism is the activation of the inflammatory cascade induced by monosodium urate fragments, which has been investigated for several years, and several studies have shown that pro-inflammatory cytokines, as well as IL-1β and TNF-α, and transcription factor, NF-κB, are essential. In the initiation and propagation of gouty arthritis induced by monosodium urate fragments [24][25][26][27][28][29]. In the pathophysiology of gouty arthritis, NF-κB signaling can encourage the production of genes encoding proinflammatory cytokines.…”

Tempuyung Leaves (Sonchus arvensis) Ameliorates Monosodium Urate Crystal-Induced Gouty Arthritis in Rats through Anti-Inflammatory Effects

“…In the pathogenesis of gouty arthritis, NF-κB signals can stimulate the production of genes that encode proinflammatory cytokines. Conversely, overexpression of TNF-α and IL-1β can directly activate the NF-κB pathway, which leads to a positive feedback loop, which further strengthens the inflammatory response and causes joint injury [14], [15], [16], [17]. Usually, NF-κB binds to the inhibiting protein, IκB and is localized in the cytoplasm.…”

Aronia melanocarpa ameliorates gout and hyperuricemia in animal models

“…The concentration of serum UA directly reflects the severity of hyperuricemia (Aksenov, Peck, Eriksson, & Stanski, 2018), and the level of XO is another important indicator directly associated with hyperuricemia (Park et al, 2018). The symptoms of hyperuricemia can be relieved when the UA level is decreased (Filler, Lopes, & Awuku, 2015;Irie et al, 2018;Pulzer et al, 2001;Zhu et al, 2018).…”