ArticleInflammopharmacology2021
Active components from Lagotis brachystachya maintain uric acid homeostasis by inhibiting renal TLR4-NLRP3 signaling in hyperuricemic mice.
Article in Inflammopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Uric Acid Causes Pancreatic β Cell Death and Dysfunction via Modulating CHOP-Mediated Endoplasmic Reticulum Stress Pathways.Diseases (Basel, Switzerland) · 2025Article
- Strategies to reduce uric acid through gut microbiota intervention.Frontiers in microbiology · 2025Review
- Plantaginis Semen Ameliorates Hyperuricemia Induced by Potassium Oxonate.International journal of molecular sciences · 2024Article
- Mechanism of flavonoids in the treatment of gouty arthritis (Review).Molecular medicine reports · 2024Review
- Gut microecology: effective targets for natural products to modulate uric acid metabolism.Frontiers in pharmacology · 2024Review
- Targeting toll-like receptor 4 (TLR4) and the NLRP3 inflammasome: Novel and emerging therapeutic targets for hyperuricaemia nephropathy.Biomolecules & biomedicine · 2023Review
- TCM and related active compounds in the treatment of gout: the regulation of signaling pathway and urate transporter.Frontiers in pharmacology · 2023Review
- Research progress on the prevention and treatment of hyperuricemia by medicinal and edible plants and its bioactive components.Frontiers in nutrition · 2023Review
- A Brief Review of Natural Products with Urate Transporter 1 Inhibition for the Treatment of Hyperuricemia.Evidence-based complementary and alternative medicine : eCAM · 2022Review
- Antibacterial and antibiofilm activity of Lagotis brachystachya extract against extended-spectrum β-lactamases-producing Escherichia coli from broiler chickens.Poultry science · 2022Article
- Active Flavonoids FromFrontiers in pharmacology · 2021Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
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.
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