Abstract
Chrysanthemum indicum Linne flower (CF) and Cinnamomum cassia (L.) J. Presl bark (CB) extracts have been used as the main ingredients in several prescriptions to treat the hyperuricemia and gout in traditional medicine. In the present study, we investigated the antihyperuricemic effects of DKB114, a CF, and CB mixture, and the underlying mechanisms in vitro and in vivo. DKB114 markedly reduced serum uric acid levels in normal rats and rats with PO-induced hyperuricemia, while increasing renal uric acid excretion. Furthermore, it inhibited the activity of xanthine oxidase (XOD) in vitro and in the liver in addition to reducing hepatic uric acid production. DKB114 decreased cellular uric acid uptake in oocytes and HEK293 cells expressing human urate transporter (hURAT)1 and decreased the protein expression levels of urate transporters, URAT1, and glucose transporter, GLUT9, associated with the reabsorption of uric acid in the kidney. DKB114 exerts antihyperuricemic effects and uricosuric effects, which are accompanied, partially, by a reduction in the production of uric acid and promotion of uric acid excretion via the inhibition of XOD activity and reabsorption of uric acid. Therefore, it may have potential as a treatment for hyperuricemia and gout.
Highlights
Hyperuricemia is characterized by elevated blood uric acid levels [1], which cause accumulation of urate crystals in joints and the kidney, leading to gout and gouty arthritis [2,3]
We found that DKB114, a combination of Chrysanthemum indicum Linne flower (CF) and CB extracts, exerted antihyperuricemic effects in rat models of potassium oxonate (PO)-induced hyperuricemia
We found that DKB114 significantly decreased serum uric acid levels in normal rats and rats with PO-induced hyperuricemia, consistent with that of our previous study and other studies [18,19,20,21]
Summary
Hyperuricemia is characterized by elevated blood uric acid levels [1], which cause accumulation of urate crystals in joints and the kidney, leading to gout and gouty arthritis [2,3]. The prevalence of hyperuricemia and gout is increasing worldwide, and uric acid is a risk factor of fatty liver, insulin resistance, hypertension, and cardiovascular diseases [4]. There is a growing interest in hyperuricemia and uric acid regulation. Hyperuricemia is caused by increased production or impaired uric acid excretion or a combination of these two mechanisms [5,6]. Reducing uric acid production and increasing uric acid excretion may be useful therapeutic approach for hyperuricemia treatment. XOD inhibitors such as Nutrients 2018, 10, 1381; doi:10.3390/nu10101381 www.mdpi.com/journal/nutrients
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