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《sh2-bβ在局灶性腦缺血再灌注大鼠頂葉皮質(zhì)的表達(dá)》由會(huì)員上傳分享，免費(fèi)在線閱讀，更多相關(guān)內(nèi)容在教育資源-天天文庫(kù)。
1、SH2-Bβ在局灶性腦缺血再灌注大鼠頂葉皮質(zhì)的表達(dá)解剖科學(xué)進(jìn)展ProgressofAnatomicalSciences2006,12(2):129～131SH2Bp在局灶性腦缺血再灌注大鼠頂葉皮質(zhì)的表達(dá)張正洪,曲鵬,齊金萍,方秀斌(中國(guó)醫(yī)科大學(xué)基礎(chǔ)醫(yī)學(xué)院神經(jīng)生物學(xué)教研室,遼寧沈陽(yáng)110001)【摘要】目的研究信號(hào)分子SH2.Bp在局灶性腦缺血再灌注大鼠大腦頂葉皮質(zhì)表達(dá)情況為闡明腦缺血的演交的分子機(jī)制從而為臨床治療提供理論依據(jù).方法用線栓法阻塞大鼠右側(cè)大腦中動(dòng)脈制作局灶性腦缺血再灌注模型,動(dòng)物隨機(jī)分為假手術(shù)組和缺血再灌注組,應(yīng)用免疫組織化學(xué)SABC法和圖像分析方法檢測(cè)大
2、鼠頂葉皮質(zhì)SH2.B13表達(dá)情況.結(jié)果假手術(shù)組右側(cè)頂葉皮質(zhì)SH2一BB有很少的表達(dá),而缺血再灌注組3h時(shí)間點(diǎn)SH2.B13在右側(cè)頂葉皮質(zhì)的平均光密度值比假手術(shù)組明顯增高,持續(xù)到24h,到48h時(shí)間點(diǎn)開(kāi)始下降,到72h已逐漸下降但仍高于假手術(shù)組(P<0.05).結(jié)論局灶性腦缺血再灌注大鼠頂葉皮質(zhì)SH2一BI3被誘導(dǎo)而表達(dá)增高,SH2.B13可能參與NGF對(duì)缺血神經(jīng)元的保護(hù)作用機(jī)制,促進(jìn)神經(jīng)元存活和損傷的修復(fù).【關(guān)鍵詞】SH2一BB;腦缺血;神經(jīng)生長(zhǎng)因子(NGF);大鼠【中圖分類號(hào)】R743.31【文獻(xiàn)標(biāo)識(shí)碼】A【文章編號(hào)】1006—2941(2oo6)o2—012
3、9—03ExpressionofSH2-BI3inPadetalLobeofFocalCerebralIschemia/ReperfusionRatsZHANGZheng?hong,QUPeng,QIJin?ping,FANGXiu?bin'(DepartmentofNeurobiology,BasicMedicalCdl~e,ChinaMedicalUniversity,Liaoningshelang110001China)【Abstract】ObjectiveTostudytheexpressionofthesignalmolecular-SH2.B13infoc
4、alcerebralischemia/reperfusion(I/R)ratsandexplorethemolecularmechanismofI/R.Me~odsFocalcerebralI/RmodelW88in.ducedbyocclusionoftherlshtmiddlecerebralarteryusingtheintraluminalsuturemethod.ThemalemrsweredividedintoshalllgroupandcerebralI/Rgrouprandomly.TheexpressionofSH2-BBWasdetectedwit
5、himmunohistoehemis-trySABCmethodandanalyzedbyimageanalysissystem.ResultsPositiveproductofSH2一B13intheshamgroupw聃barelydetected.In~ntrast,there惴amarkedincreaseoftheaverageopticaldensity(AOD)ofSH2一BB3hrsreperfusionfollowing2hrsmiddlecerebralarteryocclusion(MCAO),andthistrendcontinuedto24h
6、rsrepeffusionandbegantodecrease48hrsrepeffusion.TheaverageopticaldensityofSH2一BI3reducedmarkedlybutWasstillhig}I-erinisehemie咖with72hrsrepedusionthaninshamgroup(P<0.05).ConclusionTheoverexpressionoftSH2.B13inparietallob~afterfocalcerebralI/Rind【ieatesthatitprobablyinvolvesinthemechan
7、ismofNGFmediatedprotectiveroleforischemieneurons.【Keywords】SH2一B13;cerebralischemia;nervegrowthfactor(NGF);ratSH2一BI3,一個(gè)新近才鑒定的與細(xì)胞膜相連的銜接蛋白,在NGF誘導(dǎo)PC12細(xì)胞分化,NGF介導(dǎo)軸突生長(zhǎng)和交感神經(jīng)元存活過(guò)程中需要SH2一S13的參與,SH2一S13參與NGF的信號(hào)轉(zhuǎn)導(dǎo)過(guò)程,為NGF信號(hào)轉(zhuǎn)導(dǎo)通路上的一個(gè)重要信號(hào)蛋白[1-2】.NGF具有預(yù)防細(xì)胞凋亡,促進(jìn)神經(jīng)細(xì)胞存活和再生,使受損傷的細(xì)胞恢復(fù)正常形態(tài)和功能的作用.NG
