Abstract
Hyperuricemia is the main cause of gout and involved in the occurrence of many other diseases such as hyperlipidemia and hypertension correlated with metabolic disorders. Chrysin is a flavonoid compound found naturally in honey, propolis, and mushrooms and has anti-inflammatory and antioxidant effects. However, its mechanism of action is not clear yet. This study investigated the mechanism of chrysin’s anti-hyperuricemic effect in hyperuricemia-induced rats fed with high-fructose corn syrup. Orally administrated chrysin for 28 consecutive days effectively decreased uric acid by inhibiting the activity of xanthine oxidase (XO) in the liver. Moreover, chrysin markedly downregulated the protein expression of uric acid transporter 1 (URAT1) and glucose transporter type 9 (GLUT9) and upregulated the protein expression of organic anion transporter 1 (OAT1) and human ATP-binding cassette subfamily G-2 (ABCG2). In addition, chrysin showed prominent anti-oxidative and inflammatory effects as the malondialdehyde (MDA) and interleukin 1 beta (IL-1β) concentration was reduced in both rat kidney and serum, which aligned with the inhibition of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome signaling pathway activation. Collectively, our results strongly suggest that chrysin exhibits potent anti-hyperuricemic and anti-inflammatory effects that may yield new adjuvant treatments for gout.
Highlights
This article is an open access articleHyperuricemia occurs due to an imbalance in uric acid metabolism with accumulated serum uric acid (UA) that exceeds the saturation concentration (6.4–7.0 mg/dL) and results in many diseases including gout [1], chronic kidney disease (CKD) [2,3], cardiovascular disease [4], and metabolic syndrome [5]
In this study, we investigated the anti-hyperuricemic effects of chrysin as well as its mechanism including its regulation of urate-related transporter proteins and oxidative inflammasome activation
Effects of Chrysin on Food Intake, Fluid Intake, Body Weight, and Metabolic Markers in Following the treatment with either chrysin or allopurinol by oral gavage once daily for four weeks (Figure 1A), there was no change in tissue weight, tissue index, or kidney histology appearance (Supplementary Table S1 and Figure 1), indicating no apparent toxicity effect from chrysin treatment
Summary
Hyperuricemia occurs due to an imbalance in uric acid metabolism with accumulated serum uric acid (UA) that exceeds the saturation concentration (6.4–7.0 mg/dL) and results in many diseases including gout [1], chronic kidney disease (CKD) [2,3], cardiovascular disease [4], and metabolic syndrome [5]. Results from the 2013–2016 Nutrition and Health Study in Taiwan (NAHSIT) showed that more than 80% of Taiwanese aged from 19 to 44 consumed more than one sugar-sweetened beverage per day [9] These high-fructose-content beverages increase fructose metabolites, with subsequent consumption of a large amount of adenosine triphosphate, and an increase in the production of uric acid. It was mentioned that, in an adenine-induced chronic kidney disease rat model, the intervention of chrysin had a protective effect on the kidneys by reducing the concentration of serum creatinine (CRE), blood urea nitrogen (BUN), and tumor necrosis factor alpha (TNF-α) [24]. In this study, we investigated the anti-hyperuricemic effects of chrysin as well as its mechanism including its regulation of urate-related transporter proteins and oxidative inflammasome activation
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