酪氨酸硝基化在分泌性中耳炎所致耳蜗损伤作用实验观察

发布时间：2019-05-20 10:31

【摘要】：目的通过观察3-硝基酪氨酸(3-nitrotyrosine,3-NT)在分泌性中耳炎(Otitis Media with Effusion,OME)大鼠内耳的定位、分布及内耳组织形态学特征,确定OME大鼠耳蜗中的酪氨酸硝基化情况,探寻OME导致内耳损伤的酪氨酸硝基化机制。方法将40只健康成年雄性SD大鼠一侧耳通过阻塞咽鼓管的方法构建分泌性中耳炎模型。造模成功后分组行耳蜗石蜡切片HE染色和免疫组织化学,Tunel凋亡检测和神经节细胞的透射电镜观察。采用SPSS16.0软件包进行统计学分析,以p0.05作为有显著性差异。结果造模后大鼠的耳蜗毛细胞没有明显的缺失,HE染色发现中耳及内耳慢性炎症改变,免疫组化检测3-NT在耳蜗毛细胞、血管纹、神经纤维细胞、神经节细胞均有阳性表达,而对照组在相应部位均阴性表达。Tunel凋亡检测见耳蜗的神经纤维细胞、神经节细胞出现凋亡。透射电镜观察示神经节细胞线粒体肿胀、出现空泡化,并有神经节细胞间质的淋巴细胞浸润。结论通过构建OME模型初步发现OME能够导致耳蜗损伤,OME可能通过酪氨酸硝基化作用导致耳蜗毛细胞的凋亡、螺旋神经节细胞及神经纤维的变性,即酪氨酸硝基化是OME导致耳蜗损伤的可能机制之一。
[Abstract]:Objective To study the localization and distribution of 3-nitrotyrosine (3-NT) in the inner ear of the rat with secretory otitis media (OME) and the morphological characteristics of the inner ear. To explore the mechanism of tyrosine nitrosation of the inner ear injury caused by OME. Methods Forty healthy adult male SD rats were given a model of secretory otitis media by blocking the Eustachian tube. The paraffin sections of the cochlea were stained with HE and immunohistochemistry, and the apoptosis and the transmission electron microscope of the ganglion cells were observed after the model was successfully constructed. Statistical analysis was performed using the SPSS16.0 software package, with a significant difference in p0.05. Results There was no obvious deletion of the hair cells in the cochlea of the rats after the model, and the changes of the chronic inflammation of the middle ear and the inner ear were found by HE staining. The expression of 3-NT in the cochlear hair cells, the veins, the nerve fiber cells and the ganglion cells was detected by immunohistochemistry, and the control group was negative in the corresponding part. Tunel apoptosis was found in the nerve fiber cells of the cochlea, and the ganglion cells were apoptosis. The transmission electron microscope (TEM) observed the swelling of the mitochondria in the ganglion cells, vacuolation, and the infiltration of the cells of the ganglion cells. Conclusion OME can lead to the damage of the cochlea by constructing the OME model. OME may lead to the apoptosis of the hair cells of the cochlea, the degeneration of the spiral ganglion cells and the nerve fibers, that is, the tyrosine nitrating is one of the possible mechanisms of the OME to lead to the damage of the cochlea.
【作者单位】：南京大学医学院附属鼓楼医院耳鼻喉科;河北省邢台眼科医院耳鼻喉科;
【基金】：南京市医学发展重点项目(ZKX-07006)
【分类号】：R965

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