作者: Daniel Labbé , Masa-aki Teranishi , Alexander Hess , Wilhelm Bloch , Olaf Michel
DOI: 10.1016/J.HEARES.2004.10.002
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摘要: The aim of this study was to investigate the involvement oxidative stress and apoptosis in an animal model Meniere's disease. Endolymphatic hydrops (ELH) is generally accepted as decisive histological characteristic Closure endolymphatic duct (Kimura's method) used induce guinea pigs. Sham-operated animals served controls. After 4 weeks operated showed a significant elevation hearing thresholds measured by audiometric brainstem responses (ABR) pre- postoperatively. Immediately after second ABR measurement, were sacrificed for further immunohistological examinations inner ear with specific antibodies active caspase-3 (cas-3) marker 8-isoprostane (8-iso) nitrotyrosine (NT) indicators stress. Compared sham-operated controls, hydropic cochleae strong immunostaining both markers spiral ganglion cells, blood-vessels fibrocytes lateral wall, well supporting cells organ Corti. Activation cas-3 wall found exclusively cochleae. Our findings suggest that involved development may lead cellular damage which induces activation cas-3. Apoptotic cell death might contribute sensorineural loss later stages