【摘要】 目的 :观察JNK在丁胺卡那霉素中毒后豚鼠毛细胞的激活表达。方法 :健康豚鼠随机分为实验组和对照组各 6只 ,分别行 30 0mg·kg-1·d-1丁胺卡那霉素和生理盐水肌注。 8d后处死 ,处死前检测其畸变产物耳声发射(DPOAE)幅值变化。左耳铺片 ,右耳冰冻切片。用免疫组织化学方法检测JNK在毛细胞中的激活表达情况。结果 :对照组DPOAE幅值无明显改变 ,冰冻切片中Cortis器无JNK激活表达 ,耳蜗铺片内、外毛细胞正常。实验组DPOAE幅值明显下降 ,与对照组对比有显著性差异 (P <0 .0 1) ,冰冻切片中Cortis器中外毛细胞P JNK表达阳性 ,而内毛细胞、支持细胞无表达。耳蜗铺片显示外毛细胞大部分受损。结论 :JNK激活能够在丁胺卡那中毒后豚鼠外毛细胞中表达 ,在耳蜗损害机制中发挥重要作用更多还原

【Abstract】 Objective: Our aim was to study the effect of amikacin on the activation of JNK expression in guinea pigs. Methods:Animals were divided into 2 groups with 6 in each group.Animals in experimental group and control group received amicakin(300mg·kg -1 ·d -1 )and saline separately. After 8 days, the amplitude of DPOAE were measured before the animals were killed. Left and right cochlea were taken for cochlear preparation and cochlea frozen section respectively. The expression of JNK was detected with immunohistochemistry. Results: In control group ,the expression of P JNK was negative in the cortis organ. Cochlear preparation indicated that cells were normal. The amplitude of DPOAE did not change.In the exprimental group, the expression of P JNK was positive in out hair cell. Cochlear preparation indicated the out hair cells were impaired. The amplitude of DPOAE decreased (P<0.01). Conclusion:Activation of JNK could express in out hair cells of guinea pigs with amikacin ototoxicity,which takes a very importment part in cochlear injury .更多还原