畢業(yè)論文--催產(chǎn)素預(yù)處理對(duì)胎鼠海馬腦片缺氧無(wú)糖損傷后otr、gabaarβ表達(dá)的影響

《畢業(yè)論文--催產(chǎn)素預(yù)處理對(duì)胎鼠海馬腦片缺氧無(wú)糖損傷后otr、gabaarβ表達(dá)的影響》由會(huì)員上傳分享，免費(fèi)在線(xiàn)閱讀，更多相關(guān)內(nèi)容在學(xué)術(shù)論文-天天文庫(kù)。

1、催產(chǎn)素預(yù)處理對(duì)胎鼠海馬腦片缺氧無(wú)糖損傷后OTR、GABAARβ1表達(dá)的影響【摘要】目的：研究催產(chǎn)素(OT)預(yù)處理對(duì)胎鼠海馬腦片缺氧無(wú)糖損傷后催產(chǎn)素受體(OTR)、γ氨基丁酸A受體β1亞基(GABAARβ1)表達(dá)的影響，探討OT神經(jīng)保護(hù)的作用機(jī)制。方法：采用胎齡20dSD大鼠海馬腦片，實(shí)驗(yàn)組經(jīng)含10-6mol·L-1OT人工腦脊液(ACSF)孵育預(yù)處理后行缺氧無(wú)糖損傷(OGD)，對(duì)照組經(jīng)正常ACSF孵育后直接行OGD，各15min，SP免疫組化法半定量測(cè)定海馬CA1區(qū)OTR、GABAARβ1表達(dá)變化，電鏡觀(guān)察神經(jīng)元損傷情況。結(jié)果：實(shí)驗(yàn)組海馬CA1區(qū)OTR、GABA

2、ARβ1表達(dá)均顯著高于對(duì)照組(t=2.118、P=0.048;t=2.272、P=0.036)。對(duì)照組大量神經(jīng)元受損,核固縮或碎裂，部分核膜溶解，實(shí)驗(yàn)組細(xì)胞核、粗面內(nèi)質(zhì)網(wǎng)、線(xiàn)粒體均較對(duì)照組有所改善,核膜較光滑,胞漿腫脹較對(duì)照組減輕。結(jié)論：OT上調(diào)胎鼠海馬OTR、GABAARβ1表達(dá)，減少神經(jīng)元變性壞死，增強(qiáng)大腦耐受缺氧損傷的能力，對(duì)胎兒中樞神經(jīng)系統(tǒng)起保護(hù)作用?！娟P(guān)鍵詞】催產(chǎn)素;海馬;缺氧無(wú)糖損傷;催產(chǎn)素受體;γ氨基丁酸A受體β1亞基　　[Abstract]Objective：Tostudytheeffectsofoxytocin(OT)onchangesofox

3、ytocinreceptor(OTR),12gammaamimobutyricacidreceptorAβ1subunit(GABAARβ1)expressionsinfetusrathippocampusinducedbyoxygenandglucosedeprivation(OGD),andtoinvestigatethemechanismofneuroprotectiveeffectsofOT.Methods：Gestationalage20daysSDrathippocampusslicesintheexperimentalgroupunderwentp

4、retreatmentincubationbycontaining10-6mol·L-1OTartificialcerebrospinalfluid(ACSF),thecontrolgroupwereincubatedwithnormalACSF.Oxygenandglucosedeprivation(OGD)wasdonefor15min,respectively.SPimmunohistochemistryandsemiquantitativetechniqueweretakentodeterminehippocampusCA1areaOTR,GABAARβ1

5、expressions,andobserveneuronaldamageinelectronmicroscopy.Results:TheexpressionsofOTR,GABAARβ1inCA1areaofhippocampusweresignificantlyhigherintheexperimentalqroup(t=2.118,P=0.048;t=2.272,P=0.036).Alargenumberofdamagedneurons,nuclearcondensationorfragmentation,someofthenuclearmembranedis

6、solvedinthecontrolgroup;whilenuclei,roughendoplasmicreticulum,mitochondriawereimproved,nuclearmembranewassmooth,cytoplasmicswellingwereeasedintheexperimentalgroup.Conclusion:OTcanincreasehippocampalOTR,GABAARβ1expressions,decrease12neuronaldegenerationandnecrosis,enhancethecapacityoft

7、hebraintolerancetohypoxia,andplaytheprotectiveeffectsonfetalnervoussystem.　　[Keywords]oxytocin;hippocampus;oxygenandglucosedeprivation;oxytocinreceptor;gammaamimobutyricacidreceptorAβ1subunit　　新生兒缺氧缺血性腦病(hypoxicischemicencephalopathy,HIE)是圍產(chǎn)期缺氧、窒息導(dǎo)致腦的缺氧缺血性損害，臨床出現(xiàn)一系列中樞神經(jīng)系統(tǒng)異常表現(xiàn)的疾病，是引起

8、新生兒死亡