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浅论基质金属蛋白酶9在哮喘大鼠中性粒细胞中的表达【摘要】目的:观察基质金属蛋白酶9(MMP-9)在哮喘大鼠血中性粒细胞(PMN)中的表达,探讨PMN能否通过合成MMP-9参与哮喘的发病。方法:健康雄性SD大鼠30只,随机分成哮喘组、布地奈德治疗组和正常对照组,用卵蛋白致敏和激发的方法建立哮喘模型。分离纯化血PMN,免疫细胞化学法检测MMP-9的表达水平,ELISA法检测血清基质金属蛋白酶抑制剂-1的浓度。结果:A组PMNMMP-9的表达水平显着高于C组,B组PMNMMP-9的表达水平显着低于A组但高于C组。A组血清TIMP-1为(±)ng/mL,表达水平显着高于C组的(±)ng/mL,B组血清TIMP-1的表达水平显着低于A组但高于C组。MMP-9与TIMP-1的表达水平呈显着正相关(n=29,r=,P)。结论:哮喘大鼠PMN合成MMP-9的功能增加,PMN可能部分通过增加合成MMP-9参与哮喘的发病,这种功能可以部分被布地奈德所抑制。【关键词】哮喘;MMP-9;TIMP-1;PMN;大鼠Abstract:Objective:Toobservetheexpressionsofmatrixmetalloproteinase-9(MMP-9)inbloodpolymorphonuclearleukocyte(PMN)ofasthmaticrats.AndtoapproachwhetherPMNcouldparticipateinasthmapathogenesisthroughsynthesizingMMP-9.Methods:Thirtyratswererandomlydividedintothreegroupsonaverage,includingasthmaticgroup(groupA),budesonidetreatedgroup(groupB)andcontrolgroup(groupC).BloodPMNwereisolatedandpurified.TheexpressionsofMMP-9weredetectedwithimmunocytochemicalmethodinbloodPMN.Theconcentrationofmatrixmetallo-proteinaseinhibitor-1(TIMP-1)wasdetectedwithELISA.Results:ThelevelofMMP-9ingroupAweresignificantlyhigherthanthoseingroupC(P).LevelsofMMP-9ingroupBweresignificantlylowerthanthoseingroupA,buthigherthanthoseingroupC(allP).LevelsofTIMP-1ingroupAweresignificantlyhigherthanthoseingroupC(P).LevelsofTIMP-1ingroupBweresignificantlylowerthanthoseingroupA,buthigherthanthoseingroupC.TherewassignificantpositivecorrelationbetweenthelevelofMMP-9andTIMP-1(n=29,r=,P).Conclusion:LevelsofMMP-9synthesizedbyPMNincreaseinasthmarats.PMNmaybeimplicatedwithasthmapathogenesisviaincreasingsynthesisofMMP-9,butthisfunctionofPMNcanbepartlyinhibitedbybudesonide.Keywords:asthma;matrixmetalloproteinase-9;TIMP-1;polymorphonuclearleukocyte;rat支气管哮喘是一种由多种炎性细胞和细胞组分参与的气道慢性炎症,气道重构和气道高反应性是其特征性病理改变。基质金属蛋白酶9(matrixmetalloproteinase-9,MMP-9)及其抑制剂——