引用大鼠ELISA科研检测试剂盒的文献
文献收集：
Epimedium
引用大鼠ELISA科研检测试剂盒的文献（大鼠elisa试剂盒说明书）
AqueousExtract
AmelioratesCerebral
Ischemia/ReperfusionInjury
throughInhibitingROS/NLRP3-
MediatedPyroptosis
引用试剂盒：
种属:大鼠
IL-1β(RJ15465),IL-18(RJ15463),TNF-α(RJ16622),IL-6(RJ15478),IL-10(RJ15453),iNOS(RJ16565),MDA(RJ15503),ROS(RJ15780),CAT(RJ15737),SOD(RJ16691),GSHPx(RJ25745),LDH(RJ16172)
IF：7.675
Abstract:
Cerebralischemia/reperfusioncausesexacerbatedneuronaldamageinvolvingexces
siveneuroinflammationandoxidativestress.ROSisconsideredasignalmoleculetoactivate
NLRP3;thus,theROS/NLRP3/pyroptosisaxisplaysavitalroleinthepathogenesisofcerebralis
chemia/reperfusioninjury(CIRI).Therefore,targetingtheinhibitionoftheROS/NLRP3/pyroptosis
axismaybeapromisingtherapeutictacticforCIRI.
Epimedium
(EP)containsmanyactiveingredients
(ICA,ICSII,andICT),whichhaveawiderangeofpharmacologicalactivities.However,whether
EPcanprotectagainstCIRIremainsunknown.Thus,inthisstudy,wedesignedtoinvestigate
theeffectandpossibleunderlyingmechanismofEPonCIRI.Theresultsshowedthattreatment
withEPdramaticallymitigatedbraindamageinratsfollowingCIRI,whichwasachievedbysup
pressingmitochondrialoxidativestressandneuroinflammation.Furthermore,weidentifiedthe
ROS/NLRP3/pyroptosisaxisasavitalprocessandNLRP3asavitaltargetinEP-mediatedprotection.
Mostinterestingly,themaincompoundsofEPdirectlybondedwithNLRP3,asreflectedbymolec
ulardocking,whichindicatedthatNLRP3mightbeapromisingtherapeutictargetforEP-elicited
cerebralprotection.Inconclusion,ourfindingsillustratethatICSIIprotectsagainstneuronlossand
neuroinflammationafterCIRIbyinhibitingROS/NLRP3-mediatedpyroptosis.
