Journal of ethnopharmacology · 2026
Extract of Clematis hexapetala regulates uric acid metabolism, alleviates renal inflammation and fibrosis via the PI3K/AKT/NF-κB signaling pathway, and improves hyperuricemia in mice.
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Wang Weichao, Min Zhiqiang, Luo Chuang, Yang Min, Chen Lin
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Hyperuricemia can lead to various diseases including hyperuricemic nephropathy and gout, which result from long-term uric acid accumulation. Clematis hexapetala Pall. is one of the official species of the traditional Chinese herbal medicine Weilingxian (Clematidis Radix et Rhizoma), and it exerts significant effects in dispelling wind-dampness and anti-inflammation.
PURPOSE: To investigate the alleviative and therapeutic effects of the aqueous extract (CHP), petroleum ether fraction (CHP-PE), ethyl acetate fraction (CHP-EA), and n-butanol fraction (CHP-B) of Clematis hexapetala Pall. on hyperuricemic mice and their possible mechanisms.
METHODS: Ultra-high performance liquid chromatography-quadrupole electrostatic field orbitrap mass spectrometry (UHPLC-QE-MS) was used to analyze the components of CHP, CHP-PE, CHP-EA, and CHP-B. A mouse model of hyperuricemia (HUA) was established using potassium oxonate (PO) and hypoxanthine (HX) to evaluate the anti-HUA effects of CHP, CHP-PE, CHP-EA, and CHP-B. Network pharmacology and molecular docking analyses were employed to predict the targets and signaling pathways regulated by CHP, along with the evaluation of serum uric acid (UA) levels and renal function parameters. Western blot, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and cell analysis were used to assess the expression of proteins related to UA production and excretion, oxidative stress, inflammation, and apoptosis. Fecal 16S rRNA gene sequencing was performed to analyze changes in the intestinal microbiota, thereby achieving therapeutic and alleviative effects on hyperuricemia.
RESULTS: A total of 9094 potential active compounds were identified from CHP, CHP-PE, CHP-EA, and CHP-B by UHPLC-QE-MS, mainly including flavonoids and phenolic acids. ELISA analysis showed that high-dose CHP-B significantly reduced serum uric acid levels and improved renal tissue lesions in hyperuricemic mice. Network pharmacology identified 479 drug-disease intersection targets enriched in the PI3K/AKT/NF-κB pathway. In addition, RT-qPCR and Western blot results demonstrated that high-dose CHP-B exerted a protective effect on hyperuricemic mice induced by PO and HX by inhibiting the PI3K/AKT/NF-κB pathway. 16S rRNA gene sequencing results showed that all fractions of CHP may further alleviate HUA by regulating intestinal microbiota and maintaining intestinal homeostasis.
CONCLUSION: This study is the first to demonstrate that CHP exerts anti-HUA effects through multiple mechanisms, providing new insights into the phytotherapeutic management of HUA.
PURPOSE: To investigate the alleviative and therapeutic effects of the aqueous extract (CHP), petroleum ether fraction (CHP-PE), ethyl acetate fraction (CHP-EA), and n-butanol fraction (CHP-B) of Clematis hexapetala Pall. on hyperuricemic mice and their possible mechanisms.
METHODS: Ultra-high performance liquid chromatography-quadrupole electrostatic field orbitrap mass spectrometry (UHPLC-QE-MS) was used to analyze the components of CHP, CHP-PE, CHP-EA, and CHP-B. A mouse model of hyperuricemia (HUA) was established using potassium oxonate (PO) and hypoxanthine (HX) to evaluate the anti-HUA effects of CHP, CHP-PE, CHP-EA, and CHP-B. Network pharmacology and molecular docking analyses were employed to predict the targets and signaling pathways regulated by CHP, along with the evaluation of serum uric acid (UA) levels and renal function parameters. Western blot, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and cell analysis were used to assess the expression of proteins related to UA production and excretion, oxidative stress, inflammation, and apoptosis. Fecal 16S rRNA gene sequencing was performed to analyze changes in the intestinal microbiota, thereby achieving therapeutic and alleviative effects on hyperuricemia.
RESULTS: A total of 9094 potential active compounds were identified from CHP, CHP-PE, CHP-EA, and CHP-B by UHPLC-QE-MS, mainly including flavonoids and phenolic acids. ELISA analysis showed that high-dose CHP-B significantly reduced serum uric acid levels and improved renal tissue lesions in hyperuricemic mice. Network pharmacology identified 479 drug-disease intersection targets enriched in the PI3K/AKT/NF-κB pathway. In addition, RT-qPCR and Western blot results demonstrated that high-dose CHP-B exerted a protective effect on hyperuricemic mice induced by PO and HX by inhibiting the PI3K/AKT/NF-κB pathway. 16S rRNA gene sequencing results showed that all fractions of CHP may further alleviate HUA by regulating intestinal microbiota and maintaining intestinal homeostasis.
CONCLUSION: This study is the first to demonstrate that CHP exerts anti-HUA effects through multiple mechanisms, providing new insights into the phytotherapeutic management of HUA.