阿米卡星致毒豚鼠耳蜗中p-JNK表达增强

基础医学与临床 ›› 2011, Vol. 31 ›› Issue (8): 889-893.

阿米卡星致毒豚鼠耳蜗中p-JNK表达增强

刘双月¹,王爱梅¹,许涛²,³

1. 辽宁医学院生理教研室
2.
3. 辽宁医学院

收稿日期:2010-11-17 修回日期:2011-03-21 出版日期:2011-08-05 发布日期:2011-07-13
通讯作者: 王爱梅 E-mail:aimeiwang@yahoo.com.cn
基金资助:
辽宁省教育厅科学研究计划资助项目

Enhanced expression of phosphorylated JNK of cochlea ototoxicity by amikacin -induced in guinea pig

Shuang-yue LIU¹,Ai-mei WANG¹,Tao XU³

Received:2010-11-17 Revised:2011-03-21 Online:2011-08-05 Published:2011-07-13
Contact: Ai-mei WANG E-mail:aimeiwang@yahoo.com.cn

摘要/Abstract

摘要： 目的研究阿米卡星（AMK）对豚鼠耳蜗磷酸化c-Jun氨基末端激酶（JNK）表达的影响及其耳毒性机制。方法将豚鼠分为对照组、AMK 3、7和11d组。AMK组分别每日肌肉注射AMK（400 mg/kg），对照组肌肉注射等量生理盐水。用听脑干反应（ABR）测试和耳蜗铺片异硫氰酸四甲基罗丹明（TRITC）标记的鬼笔环肽荧光染色，观察豚鼠听觉功能及耳蜗毛细胞形态；用免疫组织化学法和显微图像技术以及蛋白质印迹技术检测p-JNK在耳蜗中的表达。结果 AMK对豚鼠耳蜗毛细胞的损伤由的底转向顶转发展。AMK 3、7和11d组耳蜗外毛细胞p-JNK阳性反应的平均吸光度值分别为169.40±1.18、153.87±2.05和145.23±2.98，AMK组p-JNK表达明显增强（P＜0.01）。在4KHz、12KHz和24KHz刺激频率下，AMK 7和11d组ABR阈移分别为6.25±1.96、10.58±2.90、16.13±3.80和49.19±7.48、58.42±7.56、63.54±8.72，比对照组显著增大（P＜0.01）。结论 JNK信号通路可能参与了AMK的耳毒性损伤。

关键词: c-Jun氨基末端激酶, 阿米卡星, 豚鼠, 耳蜗

Abstract: Objective To investigate the effect of amikacin (AMK) on the expression of phosphorylated JNK (p-JNK) in hair cells of guinea pig cochlea and the mechanism of AMK ototoxicity. Methods Guinea pigs were assigned to control group, AMK 3, 7 and 11 days group. Animals from AMK groups were daily received intramuscular injection of AMK (400 mg/kg) , while control animals were received an equivalent volume of saline. Auditory brainstem response (ABR) test and tetramethylrhodamine isothiocyanate (TRITC) -labeled phalloidine staining were used to observe the auditory function and hair cells morphology. immunohistochemistry and imaging analysis technique and Western blot were used to detect the expression of p-JNK in the cochlea. Results The hair cells missing was increased in the basal turn of cochlea and developed to the second turn. The expression of p-JNK was greater remarkably in AMK groups. And the ABR thresholds shifts increase significantly than the control group (P＜0.01) . Conclusion JNK signal pathway might participate in AMK- induced ototoxicity.

Key words: c-Jun N-terminal kinase, Amikacin, Guinea pig, Cochlea

中图分类号:

R 764.43

刘双月王爱梅许涛. 阿米卡星致毒豚鼠耳蜗中p-JNK表达增强[J]. 基础医学与临床, 2011, 31(8): 889-893.

Shuang-yue LIU Ai-mei WANG Tao XU. Enhanced expression of phosphorylated JNK of cochlea ototoxicity by amikacin -induced in guinea pig[J]. Basic & Clinical Medicine, 2011, 31(8): 889-893.

[1]	刘丽华房彩霞邓永贵周红. JNK信号通路介导高糖诱导的大鼠心肌成纤维细胞增殖[J]. 基础医学与临床, 2013, 33(2): 199-204.
[2]	黄名威唐乾利赫军俞渊王清坚黄玮. 豚鼠胆汁酸盐输出泵（BSEP）基因克隆及其在胆结石豚鼠肝组织中的表达分析[J]. 基础医学与临床, 2010, 30(7): 673-676.
[3]	林立李昌崇苏苗赏管小俊张维溪王晓丽罗运春. JNK磷酸化在哮喘大鼠肺内的动态变化[J]. 基础医学与临床, 2008, 28(2): 189-190.