石杉碱甲对D-半乳糖诱导的老年性聋大鼠听觉中枢Kir4.1表达的影响  

Effect of huperzine A on expression of Kir4.1 in auditory cortex of presbycusis rats induced by D-galactose

作　　者：孔德秋[1] 顾健[1] 阮清伟[2] 敖华飞[1] 

机构地区：[1]上海交通大学医学院附属第三人民医院耳鼻喉科,上海201900 [2]复旦大学附属华东医院中心实验室,上海200040

出　　处：《中国眼耳鼻喉科杂志》2013年第1期6-10,共5页Chinese Journal of Ophthalmology and Otorhinolaryngology

摘　　要：目的研究石杉碱甲(HupA)对D-半乳糖(D-gal)诱导的老年性聋大鼠听皮质和下丘内Kir4.1表达的影响。方法出生后3～4周Sprague-Dawley雄性大鼠45只,随机平均分为3组。D-gal组用5%D-gal(200mg/kg)对大鼠行颈背部皮下连续注射,共8周;D-gal+HupA组大鼠颈背部皮下注射同体积5%D-gal(200mg/kg)和HupA(0.1mg/kg),共8周;对照组予同体积生理盐水颈背部皮下注射,共8周。用药前、后分别检测大鼠听性脑干反应(ABR)以评价其听觉敏感度和听觉传入通路中的传导功能;利用Western印迹和免疫组织化学方法检测Kir4.1在大鼠听皮质和下丘中的表达。结果与对照组相比,D-gal组和D-gal+HupA组大鼠用药前后ABR阈值无明显改变,但两组动物ABR各频率Ⅲ、Ⅴ波潜伏期,Ⅰ-Ⅴ波间期较对照组延长(P<0.01;P<0.05),其中D-gal组ABR各频率Ⅲ、Ⅴ波潜伏期,Ⅰ-Ⅴ波间期长于D-gal+HupA组,差异有统计学意义(P均<0.05)。Western印迹结果显示:与对照组相比,D-gal组听皮质、下丘内Kir4.1蛋白表达水平明显降低(P<0.01),D-gal+HupA组Kir4.1蛋白表达与对照组无明显差异,D-gal组和D-gal+HupA组比较,Kir4.1蛋白表达差异有统计学意义(P<0.05)。下丘组织免疫荧光支持Westernblot结果。结论 HupA可以提高D-gal致老年性聋大鼠听觉中枢内Kir4.1蛋白表达,对预防和治疗老年性聋引起的听觉中枢Kir4.1减少有重要作用。Objective To investigate the effect of Huperzine A （HupA） on expression of Kir4. 1 in auditory cortex of presbycusis rats induced by D-galactose （D-gal）. Methods A total of 45 Sprague-Dawley male rats were used in the study. The rats were randomly divided into three groups. 0） D-gal group： rats were daily subcutaneously injected with 200 mg/kg D-gal for 8 weeks ;（~）Control group： rats were given the same volume of saline; （~） D-gal ＋ HupA group： rats were received both D-gal （200 mg/kg）and HupA （0. 1 mg/kg）in the same way. Central auditory function was evaluated by auditory brainstem response （ABR） before and after the treatment. Western blotting analyse and immunohistochemistry were performed to detect the expression of Kir4. 1 in auditory cortex （AC） and inferior colliculus （IC）. Results The thresholds of ABR in the three groups all showed no significant change after treatment. However, compared with the control group, the ABR latency（wave m and wave V） and I-V interpeak latency in both drug groups were delayed （ P 〈0.01 ; P 〈0.05 ） , and the latency in D-gal group was much longer （ P 〈 0.05 ）. Compared with the D-gal group, the D-gal ＋ HupA group showed increased expression of Kir4.1 （P 〈 0.05 ）. The distribution of Kir4.1 in IC was not significantly different between the control group and the D-gal ＋ HupA group, which supported the results of the western blotting. Conclusions HupA could enhance the expression of Kiv4.1 in auditory cortex of presbycusis rats induced by D-galactose, which might play an important role in preventing and treating the presbycusis-induced Kir4. 1 decreasing in auditory center. （Chin J Ophthalmol and Otorhinolaryngol,2013 ,13 ：6-10）

关 键 词：石杉碱甲 D-半乳糖 老年性聋 Kir4 1 

分 类 号：R764[医药卫生—耳鼻咽喉科]