卡铂诱导的听神经病模型大鼠脑干蜗神经核细胞凋亡因子的表达变化  

Change of apoptosis factor expression in cochlear nucleus in carboplatin-induced auditory neuropathy rat

作　　者：刘静[1] 李正莉[2] 何青 黄红彦[1] 

机构地区：[1]华中科技大学同济医学院附属同济医院耳鼻咽喉头颈外科,武汉430030 [2]华中科技大学同济医学院解剖学教研室,武汉430030 [3]武汉六七二中西医结合医院内科,武汉430079

出　　处：《解剖学报》2015年第3期324-328,共5页Acta Anatomica Sinica

摘　　要：目的探讨卡铂(CBP)诱导的听神经病模型大鼠脑干蜗神经核细胞凋亡倾向及地塞米松(DEX)的神经保护作用。方法采用腹腔注射CBP制作听神经病模型。将SD大鼠随机分为3组,即生理盐水组(NS)、卡铂组(CBP)、地塞米松干预+卡铂组(DEX+CBP),每组18只,并设3d及6d时间观察点。应用免疫组织化学方法观察各组大鼠脑干蜗神经核Caspase-3免疫反应性;RT-PCR技术检测凋亡酶激活因子1(Apaf-1)mRNA含量。结果在3d及6d时间点,CBP组大鼠脑干蜗神经核腹侧核(VCN)及背侧核(DCN)Caspase-3免疫反应性及Apaf-1mRNA含量明显强于NS组及DEX+CBP组(P<0.05),DEX+CBP组脑干蜗神经核VCN及DCN内Caspase-3免疫反应性及Apaf-1 mRNA含量与NS组差异无显著性(P>0.05)。而6d时间点CBP组蜗神经核Apaf-1 mRNA含量显示强于3d时间点。结论卡铂诱导听神经损伤的同时,也可引起大鼠脑干蜗神经核细胞凋亡倾向,而地塞米松具有神经保护作用,减弱上述的凋亡效应。Objective To investigate the influence of carboplatin （CBP） on cell apoptosis in the cochlear nucleus and the nerve protection of dexamethasone （DEX） in rats. Methods CBP was used to establish the animal model of auditory neuropathy （AN） through an intraperitoneal injection. Rats were assigned to NS group, CBP group and DEX ＋ CBP group, 18 rats per group. On day 3 and day 6 post modeling, the immunoreactivity of Caspase-3 in the cochlear nucleus was detected by immunohistochemistry and the apoptotic protease activating facter 1 （ Apaf-1 ） mRNA expression was explored by RT-PCR. Results The level of immunoreactivity of Caspase-3 and expression of Apaf-1 mRNA in the ventral cochlear nucleus（VCN） and dorsal cochlear nucleus （DCN） of CBP group were significantly higher than those in NS group and DEX ＋ CBP group （P 〈0.05） , while the levels between NS group and DEX ＋ CBP group had no significant differences（P 〉 0. 05）, and the effect on day 6 was more obvious than that on day 3. Conclusion CBP can not only damage the auditory nerve but also cause cell apoptosis on the cochlear nucleus in rats, and DEX weakens the effect of apoptosis for its neuroprotection.

关 键 词：蜗神经核 听神经病 免疫组织化学 反转录-聚合酶链反应 大鼠 

分 类 号：R512.603[医药卫生—内科学]