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研究的开题报告.docxVIP

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研究的开题报告

摘要：

大脑缺血是严重的神经系统疾病，缺血前的预处理可以显著提升脑缺血后的神经保护。本研究旨在探讨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研究。采用局灶性脑缺血大鼠模型，分别预处理MyD88途径和TRIF途径，观察缺血后神经功能、脑组织病理变化和凋亡水平的变化情况。结果发现，MyD88途径预处理组的神经功能和脑组织病理变化均明显改善，凋亡水平显著下降；TRIF途径预处理组神经功能和脑组织病理变化也有所改善，凋亡水平降低。以上结果表明，MyD88途径和TRIF途径都能够通过相应的信号途径发挥缺血预处理的神经保护效应，其中MyD88更为明显。

关键词：局灶性脑缺血；MyD88途径；TRIF途径；缺血预处理。

Abstract:

Cerebralischemiaisaseriousneurologicaldisease,andpre-treatmentbeforeischemiacansignificantlyimproveneuroprotectionaftercerebralischemia.ThisstudyaimstoexplorethemechanismofMyD88pathwayandTRIFpathwayinthetoleranceoffocalcerebralischemiainpre-treatmentrats.Usingaratmodeloffocalcerebralischemia,wepre-treatedMyD88pathwayandTRIFpathwayrespectively,andobservedthechangesinneurologicalfunction,braintissuepathologyandapoptosislevelsafterischemia.TheresultsshowedthattheneurologicalfunctionandbraintissuepathologyoftheMyD88pathwaypre-treatmentgroupweresignificantlyimproved,andtheapoptosislevelwassignificantlyreduced;theneurologicalfunctionandbraintissuepathologyoftheTRIFpathwaypre-treatmentgroupwerealsoimprovedtosomeextent,andtheapoptosislevelwasreduced.TheaboveresultsindicatethatbothMyD88pathwayandTRIFpathwaycanexertneuroprotectiveeffectsthroughcorrespondingsignalpathwaysinischemicpre-treatment,andtheeffectofMyD88pathwayismoresignificant.

Keywords:focalcerebralischemia;MyD88pathway;TRIFpathway;ischemicpre-treatment.