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机构地区:[1]重庆医科大学附属第一医院耳鼻咽喉科,重庆400016 [2]重庆医科大学附属第一医院普通外科,重庆400016
出 处:《第四军医大学学报》2008年第15期1385-1387,共3页Journal of the Fourth Military Medical University
基 金:国家"十五"攻关项目(2004BA720A19-02)
摘 要:目的:建立自身免疫性内耳病的动物模型,研究NF-κB(p65)及ICAM-1的表达及意义,并探讨其可能的发病机制.方法:提取豚鼠内耳膜迷路组织为抗原,用环磷酰胺预处理豚鼠,将抗原与等量弗氏完全佐剂一起免疫豚鼠,用Western-Blot法检测NF-κB(p65)及ICAM-1在内耳的表达变化.结果:免疫豚鼠后听性脑干反应阈显著升高,内耳出现显著的炎细胞浸润,NF-κB(p65),ICAM-1的表达增强.结论:自身免疫性内耳病NF-κB(p65)的表达增加,并诱导ICAM-1表达而引发炎症反应,降低听功能.AIM: To establish an experimental autoimmune inner ear disease model and study the expressions of NF-κB( p65 ) and ICAM-1 in autoimmune inner ear disease and discuss the possible pathogenesis. METHODS: Membranous labyrinth tissues of guinea pigs were taken as antigens beforeland. The expressions of NF-κB( p65 )and 1CAM-1 in the inner ear were observed with Western-Blot methods after the guinea pigs were pre-treated by Cyclophosphamide and immunized with antigens and complete Freund's adjuvant of equivalent volume. RESULTS: Auditory brainstem response thresholds of inner ear of antigen-sensitized animals were elevated. Inflammatory cell infiltration was seen in the cochlea of the animals. The expressions of NF-κB ( p65 ) and ICAM-1 were increased. CONCLUSION: The expression of NF-κB( p65 )is increased in autoimmune inner ear disease which can induce the expression of ICAM-1, initiate inflammatory reaction and weaken hearing function.
关 键 词:核因子κB(p65) 细胞黏附分子-1 自身免疫疾病 耳蜗
分 类 号:R764.3[医药卫生—耳鼻咽喉科]
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