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1、室旁核內(nèi)血管緊張素Ⅱ?qū)Υ笫笪溉毖?再灌注后胃黏膜NF【摘要】目的研究室旁核(paraventricularnucleus,PVN)內(nèi)注射血管緊張素Ⅱ(angiotensinⅡ,AngⅡ)對大鼠胃缺血/再灌注(gastricischemia/reperfusion,GI/R)后的胃黏膜核因子κB(NF-κB)表達的影響。方法采用核團微量注射法以及夾閉大鼠腹腔動脈30min后松開動脈夾血流復(fù)灌1h的GI/R模型,計數(shù)胃黏膜損傷指數(shù)并應(yīng)用免疫組化方法檢測胃黏膜NF-κBp65的表達。結(jié)果①GI/R可引起胃黏膜損傷,PVN內(nèi)微量注射
2、AngⅡ(0.3μl含30ng)后GI/R損傷顯著減輕;側(cè)腦室注射(icv)AngⅡ受體拮抗劑洛沙坦,能阻斷AngⅡ?qū)I/R損傷的保護作用,使GI/R損傷明顯加重;②正常大鼠胃黏膜可見NF-κB表達,并主要在胞質(zhì)表達;GI/R后,NF-κB表達增多,尤其是胞核表達明顯增加;PVN內(nèi)微量注射AngⅡ后,可使胃黏膜NF-κB表達量減少;icv給予洛沙坦可阻斷AngⅡ的效應(yīng),即GI/R損傷后胃黏膜NF-κB陽性細胞數(shù)表達量增加。結(jié)論PVN內(nèi)微量注射AngⅡ?qū)Υ笫驡I/R損傷有明顯的保護作用,且該作用可被洛沙坦翻轉(zhuǎn);NF-κB在P
3、VN內(nèi)微量注射AngⅡ減輕大鼠GI/R損傷過程中可能發(fā)揮著重要作用?!娟P(guān)鍵詞】室旁核胃缺血再灌注血管緊張素核因子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)我們以往的研究表明,下丘腦室旁核(paraventricularnucleus,PVN)是調(diào)控胃缺血
8、/再灌注(GI/R)損傷特異性中樞核團之一[1-2]?,F(xiàn)已發(fā)現(xiàn),在下丘腦室旁核小細胞區(qū)內(nèi)有豐富的血管緊張素Ⅱ(angiotensinⅡ,AngⅡ)神經(jīng)元胞體,并分布有高密度的AngⅡ的Ⅰ型(AT1)受體[3],但PVN內(nèi)的AngⅡ?qū)I/R損傷是否具有調(diào)控作用尚未見報道。目前有研究顯示,胃