摘要
目的揭示线粒体能量转换功能在噪声性耳蜗毛细胞凋亡启动和进程中的作用。方法选择成年灰鼠17只,分为两组,实验组(12只)接受噪声暴露,对照组(5只)未接受噪声暴露。全部动物应用微量注射器将一种不可逆的琥珀酸脱氢酶(SDH)抑制剂3-硝基丙酸(3-NP,50mmol/L),滴入灰鼠右耳(实验耳)耳蜗圆窗膜,使其缓慢渗透到内耳以抑制细胞线粒体的能量转换功能。左耳(对照耳)耳蜗圆窗膜滴入人工外淋巴液(AP)。耳蜗圆窗膜给药后16h,将动物暴露于155dBSPL的脉冲噪声75次。噪声暴露后2h,解剖取双侧耳蜗。采用细胞核DNA荧光染料碘化丙锭(PI)染色耳蜗基底膜,荧光显微镜下观察噪声暴露后耳蜗基底膜毛细胞核的形态学变化。结果在噪声性耳蜗基底膜外毛细胞损伤区域内,实验耳可见大量中等程度核固缩、少量核碎裂的外毛细胞,而对照耳见大量核碎裂、少量中等程度核固缩的外毛细胞。结论线粒体能量转换功能在噪声诱导耳蜗毛细胞凋亡中起着重要的作用,抑制线粒体功能对强脉冲噪声诱导的耳蜗外毛细胞凋亡的启动无明显影响,但可延缓毛细胞凋亡的进程。
Objective To examine the role of mitochondrial energy-conversion efficiency in regulating the initiation and execution of the apoptotic process in outer hair cells（OHCs）of cochlea following exposure to intense noise.Methods Seventeen adult chinchillas were used in present study.The animals were randomly assigned to one of the two groups,12 animals were exposed to noise and the remaining 5 animals without exposure to noise served as normal control.For all the animals,3-nitropropionic acid solution（3-NP,50mmol/L）,an irreversible inhibitor of succinate dehydrogenase（SDH）,was dropped onto the round window of the cochlea of the right ear using a micro-syringe to inhibit the mitochondrial energy production,to serve as the test ear.Artificial perilymph solution（AP）was dropped onto the round window of the cochlea of the left ear to serve as the control ear.16h after application of 3-NP and AP,the animals were exposed to 75 pairs of impulse noise at 155 dB pSPL.The cochleae were harvested 2h after the noise exposure.The cochlear basilar membrane was stained with propidium iodide（PI）,a DNA intercalating fluorescent probe used to visualize the morphologic viability of hair cell nuclei.All the specimens were examined with a fluorescence microscope.Results In the 3-NP-treated cochlea,medium degree of nuclear condensation of OHCs appeared to be the dominant nuclear pathology,and only a few OHCs showed nuclear fragmentation in the damaged area of the cochlea.In contrast,the AP-treated control ear exhibited a large quantity of nuclear fragments,and a small quantity of medium degree of nuclear condensation.Conclusion The present study indicates that mitochondrial energy-conversion function plays an important role in regulating the apoptotic process.Disruption of the mitochondrial energy can not deter the apoptotic process from initiation,but can slow down the pace of apoptotic progression in outer hair cells of the cochlea following exposure to intense noise.
出处
《解放军医学杂志》
CAS
CSCD
北大核心
2008年第8期964-966,共3页
Medical Journal of Chinese People's Liberation Army
基金
美国NIH资助项目(NIDCD1R03DC006181-01A1)
关键词
线粒体
细胞凋亡
噪声
毛细胞
耳蜗
mitochondria
apoptosis
noise
hair cells
cochlea
作者简介
杨卫平，医学硕士，研究员。主要从事聋病的发生机制及防治研究。E-mail：yangwp2002@yahoo．com
