摘要
目的探讨豚鼠耳蜗缺血再灌注损伤时IκBα变化。方法经颅底径路建立豚鼠椎基底动脉缺血再灌注耳蜗损伤模型,采用石蜡包埋免疫组织化学染色光学显微镜下观察IκBα在耳蜗组织中的表达。结果正常对照组螺旋神经节、血管纹和Corti’s器的细胞浆内可见IкBα强阳性表达。缺血再灌注后各组上述部位表达减弱,再灌注24h最弱,48h及7d的表达有所增强。着色部位主要在胞浆,再灌注24h后可见胞核内亦有表达。正常组与缺血再灌注各组比较灰度值有统计学意义(P<0.01)。结论耳蜗缺血再灌注损伤时可能存在IkBα的降解和核转位。
Objective To investigate the changes of expression of IκBα in the cochlea of guinea pigs induced by vertebrobasilar artery ischemia reperfusion. Methods The model of vertebrobasilar artery ischemia reperfusion was established via the skull base approach. The spatial and temporal features of IκBα induction following ischemia reperfusion were studied by paraffin-embedded immunohistochemistry. Results The positive teaetion of IκBα was found in the cytoplasm of Corti ' s organ, spiral ganglion cells ( SGCs ) , and stria vasucularis in normol control group. After ischemia and reperfusion, the expression was gradually decreasing and reached the weakest at 24 hours, but re-upregulated 48 hours and 7 days after reperfusion. The expression of IκBα immunoreactivity was prominent in the cytoplasm. Positive immunoreaetivity could also be observed in the nucleus 24 hours after reperfusion. Image analysis showed that the differences of expression between the normol control group and the reperfusion groups were statistically significant ( P 〈 0. 01 ). Conclusion The degradation of IκBα and the nuclear translocation can be demonstrated during the ischemia reperfusion of cochlea.
出处
《中国耳鼻咽喉颅底外科杂志》
CAS
2010年第5期341-344,共4页
Chinese Journal of Otorhinolaryngology-skull Base Surgery
关键词
耳蜗
缺血再灌注损伤
抑制因子
Cochlea
Ischemia reperfusion injury
Inhibitory factor