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Войти в исследования BMC biotechnology · 2026
Mechanistic insights into how cichoriin inhibits P2Y14R to suppress MSU-induced gouty inflammation.
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Wu Xue, Liu Shanshan, Leng Li, Liu Zhengqi
Аннотация
BACKGROUND: Gout is a prevalent, chronic inflammatory joint diseases, and its global prevalence and incidence are continue to rise. Currently, the adverse side effects of anti-gout drugs underscore the urgent need for safer and more effective anti-gout agents.
OBJECTIVE: Cichoriin is a kind of coumarin, which exhibits diversity of biological activities. The current investigation aimed to explore the mechanism of the inhibition of MSU-induced gouty inflammation by cichoriin.
METHODS: The enzyme inhibitory assay of P2Y14R, cell viability detection, ELISA, immunofluorescence staining, and flow cytometry were used to explore the molecular mechanism of cichoriin in the inhibition of MSU-induced gouty inflammation. The molecular level details of inhibitory effects of chchoriin against P2Y14R were obtained by molecular dynamics simulation.
RESULTS: The in vitro experiments revealed that cichoriin could inhibit the activity of P2Y14R, up-regulate the expressions of NLRP3, Caspase-1, GSDMD and ASC, increase IL-1β and IL-18 levels, and decrease the percentage of Caspase-1/PI double-positive cells. The computational calculations revealed that cichoriin and P2Y14R could form a stable and rigid complex. Free energy landscape exhibited that cichoriin stabilized the global conformations of P2Y14R to the minimum global energy. MM-PBSA provided evidence for cichoriin's stability inside the binding pocket of P2Y14R with a binding free energy of -35.13 kcal/mol. The decomposition of binding energy showed the pivotal amino acids residues responsible for the stability of cichoriin's interaction with P2Y14R by forming hydrogen bonds and hydrophobic interactions.
CONCLUSIONS: This work highlighted the potential roles of cichoriin in attenuating MSU-induced gouty inflammation.
OBJECTIVE: Cichoriin is a kind of coumarin, which exhibits diversity of biological activities. The current investigation aimed to explore the mechanism of the inhibition of MSU-induced gouty inflammation by cichoriin.
METHODS: The enzyme inhibitory assay of P2Y14R, cell viability detection, ELISA, immunofluorescence staining, and flow cytometry were used to explore the molecular mechanism of cichoriin in the inhibition of MSU-induced gouty inflammation. The molecular level details of inhibitory effects of chchoriin against P2Y14R were obtained by molecular dynamics simulation.
RESULTS: The in vitro experiments revealed that cichoriin could inhibit the activity of P2Y14R, up-regulate the expressions of NLRP3, Caspase-1, GSDMD and ASC, increase IL-1β and IL-18 levels, and decrease the percentage of Caspase-1/PI double-positive cells. The computational calculations revealed that cichoriin and P2Y14R could form a stable and rigid complex. Free energy landscape exhibited that cichoriin stabilized the global conformations of P2Y14R to the minimum global energy. MM-PBSA provided evidence for cichoriin's stability inside the binding pocket of P2Y14R with a binding free energy of -35.13 kcal/mol. The decomposition of binding energy showed the pivotal amino acids residues responsible for the stability of cichoriin's interaction with P2Y14R by forming hydrogen bonds and hydrophobic interactions.
CONCLUSIONS: This work highlighted the potential roles of cichoriin in attenuating MSU-induced gouty inflammation.