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ID:21054002
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页数:4页
时间:2018-10-19
《室旁核内血管紧张素ⅱ对大鼠胃缺血-再灌注后胃黏膜nf》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NF【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
2、AngⅡ(0.3μl含30ng)后GI/R损伤显著减轻;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P
3、VN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】室旁核胃缺血再灌注血管紧张素核因子κBAbstract:ObjectiveTostudytheeffectofangiotensinⅡ(AngⅡ)intheparaventricularnucleus(PVN)ontheexpressionofNF-κBingastricmucosafolloia/reperfusion(GI/R)inrats.MethodsIntranuclearmicroinjectionandmodelofGI/Rploye
4、dintheexperiment.TheGI/Rmodelpingtheceliacarteryfor30mintoinduceischemiaandalloalsucosaldamageindexandtheexpressionofNF-κBinthegastricmucosabyimmunohistochemistry.Results①GI/Rinducedgastricmucosalinjury;microinjectionofAngⅡ(30ng)intoPVNobviouslyattenuatedtheGI/Rinj
5、ury;intracerebroventricularinjection(icv)oflosartan,anAngⅡAT1receptorantagonist,couldeliminatetheprotectiveeffectofAngⅡagainsttheI/R-inducedgastricmucosalinjury.②NF-κB(p65)ainlyexpressedinthecytoplasminthemiddleandbottomlayersofgastricmucosainnormalrat,NF-κBandtran
6、slocatedtothenucleiofgastricmucosalcellsafter1hofI/R.MicroinjectionofAngⅡ(30ng)intothePVNsignificantlysuppressedthetranslocationofp65tothenuclei,andlosartanblockedtheeffectofAngⅡ.TheexpressionofNF-κBvarieducosaldamageindex.ConclusionMicroinjectionofAngⅡintothePVNpr
7、otectsagainstGI/Rinjury,andtheprotectiveeffectofAngⅡcanbereversedbylosartan.NF-κBmayplayanimportantroleinthePVN,ediatestheprotectionagainstGI/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
8、/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
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