bmp7对大鼠脑缺血再灌注损伤后nestin和gfap表达的影响

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1、摘要目的观察骨形态发生蛋白一7(BMP-7)对大鼠局灶性脑缺血再灌注损伤的保护作用，检测应用BMP-7后缺血侧脑组织巢蛋白(nestin)和胶质纤维酸性蛋白(GFAP)表达的变化，探索BMP-7的组织保护作用及可能的机制。方法取40只成年健康雄性SD大鼠，随机分成假手术组、对照组和BMP-7治疗组，每组10只。采用线栓法制做大鼠大脑中动脉阻塞(MCAO)模型，阻塞2h后再灌，同时治疗组用微量注射器经尾静脉注射250p1BMP-7(O．1mg·kg‘1)，对照组和假手术组经尾静脉注射等量无菌注射用水。再灌注24h后按照Bederson评

2、分标准对大鼠进行神经行为功能评分，2，3，5一三苯四氮唑(TTC)染色观察大鼠脑梗死体积，HE染色观察脑组织病理变化，TUNEL法检测神经细胞凋亡，免疫组织化学方法(SABC)检测缺血脑组织内nestin和GFAP表达。结果假手术组大鼠神经行为功能正常，无脑梗死。HE染色可见脑组织神经元形态完整。假手术组大鼠脑组织TUNEL阳性细胞数量少，散在分布。免疫组化示nestin和GFAP表达很弱。BMP-7治疗组大鼠神经功能评分(t=4．66，P

3、海马及纹状体TUNEL阳性细胞数降低(P

4、(GFAP)inbraiatissueofrataftercerebralischernicreperfusion询ury．Methods：Tenratsfrom40adulthealthymaleSprague-Dawleyratsreceivedsham—operation,theotherratsweresubjectedtomiddlecerebralarteryocclusion(MCAO)for2hours，the20suez：essfullymodeledratswereequallyrandomizedintothet

5、reatmentgroupandcontrolgroup．RatsinthetreatmentgroupwereintervenedwithBMP7(0．1ing‘kgu)250rtlviacaudalveininjection，whileratsincontrolgroupandsham·operativegroupWereinjectedwithequalvolumeofsterilewaterforinjection．NeurologicaldeficitswereevaluatedbyBederson’Smethodat24h

6、afterischemia-reperfusion,theinfarctionvolumeofbrainWaSinvestigatedby2,3，5一triphenyltetrazoliumchloridecoloring．111eneuronalapoptosisWaSassassedbyTUNELstainingandtheexpressionofnestinand’GFAPofthethreegroupswasanalyzedbyimmunohistochemistrymethod．ResultsThenevousbehavio

7、ralmalfunctionwasnormalandthereWasnofocusinfarctioninshamoperativegroup．TheapoptoticcellswerescatteringinbriantissueandtheexpressionofnestinandGFAPWereweaklyintheshamoperativegroup．TheBederson’Sscore(t--4．66，P

8、entgroupthanthoseincontrolgroup．Besides，thenumberofTUNELpositivecellsintreatmentgroupWaSlowerthanthoseincontro