MyD88途径和TRIF途径在缺血预处理大鼠局灶性脑缺血耐受作用机制的分析.pdfVIP

·英文论著摘要· Themechanismresearchinratfocal - l■ l ● · l ■·- ● l ■ 1●J● cereDralischemictoleranceWitlllschemic both throughMyD88--andTRIF·-dependentpathways ective Obj The will theextra ofthecerebral majorityofneurosurgicalprocedures injury bring ischemiato the hasdramaticeffecton outcomes． patient,which surgical brain releases and Hypoxic-ischemicdamage(HIBD)isirreversible，whichcytokines freeradicalstoexacerbate oxygen ischemicbrain inflammationand damagethrough toleranceisamethodoflessthanthelethaldoseof apoptosis．Pretreatrnent drugs given in itcause mild SOasto thefatal advance，then relativelyinflammatoryresponseeasing inbrain effect．TOLL-like an mjury,resultingprotection roleinthe Can indispensable inflammatoryresponse，TLRsidentifyendogenous molecular associated damage—associated exogenous pattern(DAMP)andpathogen molecular therelated are induceNF-r,B pattern(PAAfP)，whenligandsactivated，TLRs related cytokinesthrough pathway,andproduce pro··inflammatory MyD88·-dependent interferon to pathwaypromote