期刊
INFLAMMOPHARMACOLOGY
卷 29, 期 4, 页码 1187-1200出版社
SPRINGER BASEL AG
DOI: 10.1007/s10787-021-00844-5
关键词
Luteolin; Luteoloside; Apigenin; Hyperuricemia; Uric acid transporter; Inflammation
资金
- National Natural Science Foundation of China [82060757]
- Science and Technology Research Project of Jiangxi Provincial Department of Education [GJJ190632]
- Science and Technology Project of Jiangxi Provincial Administration of Traditional Chinese Medicine [2019A004, 2019A258]
Luteolin, luteoloside and apigenin can attenuate hyperuricemia by reducing the production and increasing the excretion of uric acid, mediated by inhibiting inflammatory signaling pathways.
Lagotis brachystachya Maxim is a herb widely used in traditional Tibetan medicine. Our previous study indicated that total extracts from Lagotis brachystachya could lower uric acid levels. This study aimed to further elucidate the active components (luteolin, luteoloside and apigenin) isolated from Lagotis brachystachya and the underlying mechanism in vitro and in vivo. The results showed that treatment with luteolin and luteoloside reversed the reduction of organic anion transporter 1 (OAT1) levels, while apigenin attenuated the elevation of urate transporter 1 (URAT1) and glucose transporter 9 (GLUT9) levels in uric acid-treated HK-2 cells, which was consistent with the finding in the kidneys of potassium oxonate (PO)-induced mice. On the other hand, hepatic xanthine oxidase activity was inhibited by the components. In addition, all of these active components improved the morphology of the kidney in hyperuricemic mice. Moreover, molecular docking showed that luteolin, luteoloside and apigenin could bind Toll-like receptor 4 (TLR4) and NLR family pyrin domain containing 3 (NLRP3). Congruently, western blot analysis showed that the components inhibited TLR4/myeloid differentiation primary response 88 (MyD88)/NLRP3 signaling. In conclusion, these results indicated that luteolin, luteoloside and apigenin could attenuate hyperuricemia by decreasing the production and increasing the excretion of uric acid, which were mediated by inhibiting inflammatory signaling pathways.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据