Thepresentstudywasdesignedtoexaminetheanti-hyperuricemicandanti-inflammatoryeffectsandpossiblemechanismsofvaticaffinol,aresveratroltetramerisolatedfromethanolextractsofDipterocarpusalatus,inoxonate-inducedhyperuricemicmice.At1hafter250mg·kg~(-1)potassiumoxonatewasgiven,vaticaffinolat20,40,and60mg·kg~(-1)wasintragastricallyadministeredtohyperuricemicmiceoncedailyforsevenconsecutivedays.Vaticaffinolsignificantlydecreasedserumuricacidlevelsandimprovedkidneyfunctioninhyperuricemicmice.Itinhibitedhepaticactivityofxanthinedehydrogenase(XDH)andxanthineoxidase(XOD),regulatedrenalmRNAandproteinlevelsofuratetransporter1(URAT1),glucosetransporter9(GLUT9),organicaniontransporter1(OAT1),organiccationtransporter1(OCT1),OCT2,organiccation/carnitinetransporter1(OCTN1),andOCTN2inhyperuricemicmice.Moreover,vaticaffinolmarkedlydown-regulatedrenalproteinlevelsofNOD-likereceptor3(NLRP3),apoptosis-associatedspeck-like(ASC),andCaspase-1,resultinginthereductionofinterleukin(IL)-1β,IL-18,IL-6andtumornecrosisfactor-α(TNF-α)levelsinthisanimalmodel.Additionally,HPLCandLC-MSanalysesclearlytestifiedthepresenceofvaticaffinolinthecrudeextract.Theseresultssuggestthatvaticaffinolmaybeusefulforthepreventionandtreatmentofhyperuricemiawithkidneyinflammation.
