脑缺血再灌注致听力损伤的机制研究

发布时间：2018-02-27 11:33

本文关键词： 缺血再灌注损伤血脑屏障凋亡缝隙连接金属蛋白酶　出处：《听力学及言语疾病杂志》2017年05期 　论文类型：期刊论文

【摘要】：目的探讨大鼠局灶性脑缺血再灌注后听力损伤的机制。方法选择健康白色雄性SD大鼠60只,随机分为假手术组和缺血再灌注组,每组30只。缺血再灌注组大鼠采用线栓法制备大脑中动脉栓塞模型,脑缺血60min,再灌注24h;假手术组只分离颈部血管,不插入线栓。造模前及造模24小时后两组分别检测听性脑干反应,行神经功能评分,然后处死动物,检测脑组织含水量和脑梗死体积,通过Evans blue的渗出情况评估血脑屏障的完整性,末端标记法观察神经细胞凋亡状况,计算凋亡指数;Western blot法检测金属蛋白酶9(MMP-9)、紧密连接蛋白5(Claudin-5)、闭锁蛋白(Occludin)、连接蛋白43(CX-43)的表达。结果与假手术组比较,缺血再灌注组ABR反应阈值明显升高,神经功能评分升高,脑组织含水量增多,脑梗死体积增大,脑神经细胞凋亡指数显著增加,MMP-9、CX-43蛋白表达明显上升,Claudin-5、Occludin蛋白表达显著下降,差异均具有统计学意义(均为P0.05)。结论大鼠局灶性脑缺血再灌注脑损伤后其听力损伤可能与MMPs激活、细胞凋亡、血脑屏障破坏及缝隙连接损伤有关。
[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.
【作者单位】：河北医科大学第二医院耳鼻咽喉科;河北医科大学第二医院骨科;
【分类号】：R743.3;R764

【相似文献】