Abstract: [
Abstract ] Objective Thisstudyistoexploretheprotectiveroleand mechanism of
Acetylbritannilactone ( ABL ) oninflammatoryresponsesinducedbyfocalcerebralischemiain
mice.Methods MaleCD1 miceweresubjectedtopermanentmiddlecerebralarteryocclusion
( MCAO ) .Themicewererandomlydividedintosham-operatedgroup , MCAOgroup , ABL-L
group ( 10mg
/
kg
) andABL-Hgroup (
30mg
/
kg
) .ABLwasinjectedintraperitoneally30minutes
priortoMCAOoperation.Micewereanesthetizedandsacrificedat24hafterstroke.Western
blottingandRT-PCRwereusedtoexaminetheexpressionoftumornecrosisfactor-α ( TNF-α ),
interleukin-1 β ( IL-1 β ), Toll-likereceptor4 ( TLR4 ), tumornecrosisreceptorassociatedfactor6
( TRAF6 ) andnuclearfactor-kappaB ( NF-κB ) .Andtheneurologicaldeficitscores , brainwater
contentandinfarctvolumewereexplored.Results Comparedtoshamgroup , theexpressionsof
TNF-α , IL-1 β , TLR-4 , TRAF6andNF-κBweresignificantlyincreasedin MCAOgroup ( P <
0.05 ) .ABLtreatmentmarkedlydown-regulatedexpressionsofTNF-α , IL-1 β , TLR4 , TRAF6 ,andNF-κB ( P <0.05 ) .Theneurologicaldeficitscores , infarctvolumeandbrainwatercontent
werealleviatedcomparedto MCAOgroup ( P <0.05 ) .Conclusion ABLtreatmenteffectively
ameliorates neurological defect , brain edema and brain infarct volume.ABL decreases
inflammatory responses by suppressing the expression of the proinflammatory signaling
moleculesTLR4 , TRAF6