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腦缺血再灌注致聽力損傷的機制研究

發(fā)布時間:2018-02-27 11:33

  本文關鍵詞: 缺血再灌注損傷 血腦屏障 凋亡 縫隙連接 金屬蛋白酶 出處:《聽力學及言語疾病雜志》2017年05期  論文類型:期刊論文


【摘要】:目的探討大鼠局灶性腦缺血再灌注后聽力損傷的機制。方法選擇健康白色雄性SD大鼠60只,隨機分為假手術組和缺血再灌注組,每組30只。缺血再灌注組大鼠采用線栓法制備大腦中動脈栓塞模型,腦缺血60min,再灌注24h;假手術組只分離頸部血管,不插入線栓。造模前及造模24小時后兩組分別檢測聽性腦干反應,行神經功能評分,然后處死動物,檢測腦組織含水量和腦梗死體積,通過Evans blue的滲出情況評估血腦屏障的完整性,末端標記法觀察神經細胞凋亡狀況,計算凋亡指數(shù);Western blot法檢測金屬蛋白酶9(MMP-9)、緊密連接蛋白5(Claudin-5)、閉鎖蛋白(Occludin)、連接蛋白43(CX-43)的表達。結果與假手術組比較,缺血再灌注組ABR反應閾值明顯升高,神經功能評分升高,腦組織含水量增多,腦梗死體積增大,腦神經細胞凋亡指數(shù)顯著增加,MMP-9、CX-43蛋白表達明顯上升,Claudin-5、Occludin蛋白表達顯著下降,差異均具有統(tǒng)計學意義(均為P0.05)。結論大鼠局灶性腦缺血再灌注腦損傷后其聽力損傷可能與MMPs激活、細胞凋亡、血腦屏障破壞及縫隙連接損傷有關。
[Abstract]:Objective to investigate the mechanism of hearing loss after focal cerebral ischemia reperfusion in rats. Methods 60 healthy white male SD rats were randomly divided into sham operation group and ischemia reperfusion group. There were 30 rats in each group. The middle cerebral artery embolization model was made by the method of thread embolization in the ischemia reperfusion group, the cerebral ischemia for 60 minutes and the reperfusion for 24 hours, while the sham operation group only separated the cervical blood vessels. Before and after 24 hours of modeling, auditory brainstem response was measured, neurological function was scored, then animals were killed, brain water content and cerebral infarct volume were measured. The integrity of the blood-brain barrier was evaluated by the exudation of Evans blue, and the apoptosis of neurons was observed by the end labeling method. The expression of metalloproteinase 9 (MMP-9), tight junction protein 5 (Claudin-5), atresia protein (Occludinus) and connexin 43 (CX-43) were detected by Western blot. Results compared with sham operation group, the ABR response threshold and neurological function score of ischemia reperfusion group were significantly higher than those of sham operation group. The water content of brain tissue increased, the volume of cerebral infarction increased, the apoptotic index of cerebral nerve cells increased significantly, and the expression of MMP-9 CX-43 protein increased significantly. The expression of Claudin-5 Occludin protein decreased significantly. Conclusion the hearing loss after focal cerebral ischemia-reperfusion injury in rats may be related to MMPs activation, apoptosis, blood-brain barrier damage and gap junction damage.
【作者單位】: 河北醫(yī)科大學第二醫(yī)院耳鼻咽喉科;河北醫(yī)科大學第二醫(yī)院骨科;
【分類號】:R743.3;R764

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