室旁核内血管紧张素ⅱ对大鼠胃缺血-再灌注后胃黏膜

《室旁核内血管紧张素ⅱ对大鼠胃缺血-再灌注后胃黏膜》由会员上传分享，免费在线阅读，更多相关内容在工程资料-天天文库。

1、室旁核内血管紧张素Ⅱ对大鼠胃缺血/再灌注后胃黏膜【摘要】目的研究室旁核（paraventricularnucleus，PVN）内注射血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)对大鼠胃缺血/再灌注(gastricischemia/reperfusion,GI/R)后的胃黏膜核因子κB（NF-κB）表达的影响。方法采用核团微量注射法以及夹闭大鼠腹腔动脉30min后松开动脉夹血流复灌1h的GI/R模型，计数胃黏膜损伤指数并应用免疫组化方法检测胃黏膜NF-κBp65的表达。结果①GI/R可引起胃黏膜损伤，PVN内微量注射AngⅡ（0.3μl含30ng）后GI/R损伤显

2、著减轻；侧脑室注射（icv）AngⅡ受体拮抗剂洛沙坦，能阻断AngⅡ对GI/R损伤的保护作用，使GI/R损伤明显加重;②正常大鼠胃黏膜可见NF-κB表达，并主要在胞质表达;GI/R后，NF-κB表达增多，尤其是胞核表达明显增加;PVN内微量注射AngⅡ后，可使胃黏膜NF-κB表达量减少；icv给予洛沙坦可阻断AngⅡ的效应，即GI/R损伤后胃黏膜NF-κB阳性细胞数表达量增加。结论PVN内微量注射AngⅡ对大鼠GI/R损伤有明显的保护作用，且该作用可被洛沙坦翻转;NF-κB在PVN内微量注射AngⅡ减轻大鼠GI/R损伤过程中可能发挥着重要作用。【关键词】室旁核胃缺血再

3、灌注血管紧张素核因子κBAbstract:ObjectiveTostudytheeffectofangiotensinⅡ(AngⅡ)intheparaventricularnucleus(PVN)ontheexpressionofNF-κBingastricmucosafolloia/reperfusion(GI/R)inrats.MethodsIntranuclearmicroinjectionandmodelofGI/Rployedintheexperiment．TheGI/Rmodelpingtheceliacarteryfor30mintoinduceisch

4、emiaandalloalsucosaldamageindexandtheexpressionofNF-κBinthegastricmucosabyimmunohistochemistry.Results①GI/Rinducedgastricmucosalinjury;microinjectionofAngⅡ（30ng）intoPVNobviouslyattenuatedtheGI/Rinjury;intracerebroventricularinjection(icv)oflosartan,anAngⅡAT1receptorantagonist,couldelimi

5、natetheprotectiveeffectofAngⅡagainsttheI/R-inducedgastricmucosalinjury.②NF-κB(p65)ainlyexpressedinthecytoplasminthemiddleandbottomlayersofgastricmucosainnormalrat,NF-κBandtranslocatedtothenucleiofgastricmucosalcellsafter1hofI/R.MicroinjectionofAngⅡ(30ng)intothePVNsignificantlysuppressed

6、thetranslocationofp65tothenuclei,andlosartanblockedtheeffectofAngⅡ.TheexpressionofNF-κBvarieducosaldamageindex.ConclusionMicroinjectionofAngⅡintothePVNprotectsagainstGI/Rinjury,andtheprotectiveeffectofAngⅡcanbereversedbylosartan.NF-κBmayplayanimportantroleinthePVN,ediatestheprotectionag

7、ainstGI/Rinjury.Keyia/reperfusion(GI/R);angiotensinⅡ(AngⅡ);nuclearfactorκB（NF-κB）我们以往的研究表明，下丘脑室旁核（paraventricularnucleus，PVN）是调控胃缺血/再灌注(GI/R)损伤特异性中枢核团之一［1－2］。现已发现，在下丘脑室旁核小细胞区内有丰富的血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)神经元胞体，并分布有高密度的AngⅡ的Ⅰ型(AT1)受体［3］，但PVN内的AngⅡ对GI/R损伤是否具有调控作用尚未见报道。目前有研究显示,胃黏膜