Abstract
This study was performed to investigate the therapeutic effects and possible mechanisms of sunflower (Helianthus annuus) head extract (SHE) on gout. First, the components of sunflower head powder and SHE were analyzed systematically. SHE, especially SHEB (extracted with 20% ethanol and 80% double-distilled water), strongly suppressed the swelling of the ankles in rats with acute gout induced by monosodium urate (MSU) crystals and reduced the levels of uric acid and xanthine oxidase (XO) in mice with hyperuricemia induced by oteracil potassium and yeast extract powder. Hematoxylin and eosin staining indicated that SHEB reduced inflammation cells and increased the joint space in the ankle compared with the control rats with MSU-induced gout. In the rats with acute gout, among 13 detected inflammatory cytokines, SHEB significantly enhanced the serum levels of interleukin-10 and the monocyte chemoattractant protein 1α. In the mice with hyperuricemia, SHEB reduced the levels of glutathione peroxidase, superoxide dismutase, malondialdehyde, and nitrogen monoxide in liver tissues. The potential therapeutic effects of SHE on gout are probably due to the production of anti-inflammatory cytokines and the suppression of XO activity via the modulation of oxidative stress status.
Highlights
Gout is a common arthritic disease associated with joint pain, fatigue, and high fever [1]
It is generally agreed that gout is caused by the deposition of monosodium urate (MSU) crystals within joints characterized by chronic hyperuricemia [4]
Not including the sunflower head powder, the highest concentrations of flavonoid and triterpene were noted in SHEC and SHED, respectively (Table 1)
Summary
Gout is a common arthritic disease associated with joint pain, fatigue, and high fever [1]. The prevalence of gout is estimated at 2%; it is especially observed among men over 40 years of age with concomitant metabolic syndrome [2]. The increasing trend of gout is likely to lead to increasingly large social costs, including direct costs related to medical treatment and indirect costs associated with absenteeism and presenteeism [3]. It is generally agreed that gout is caused by the deposition of monosodium urate (MSU) crystals within joints characterized by chronic hyperuricemia (serum uric acid [UA] levels of >6.8 mg/dL) [4]. UA is the end product of purine catabolism under the catalysis of xanthine oxidase (XO) [5] and serves as the main clinical biochemical index of gout [6]. MSU crystals stimulate monocytes to produce tumor necrosis factor alpha (TNF-α) and interleukin-1β (IL-1β) and activate endothelial cells [9]
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