【摘要】 目的 探讨强噪声能否诱导豚鼠耳蜗螺旋神经节细胞(sprial ganglion cell,SGC)的凋亡,及动态观察凋亡蛋白酶Caspase-12在强噪声暴露后豚鼠耳蜗SGC损伤中的作用。方法 选用健康雄性白色豚鼠20只,将实验组豚鼠暴露在4 k Hz窄带噪声120dB SPL环境中4 h,噪声刺激停止后1、4、14 d组及对照组在处死前测听性脑干反应(每组各5只)。通过脱氧核糖核甘酸末端转移酶介导的缺口末端标记法(ternial-deoxynucleotidyl transferase mediated nick end labeling,TUNEL)检测SGC凋亡细胞,免疫组化检测Caspase-12蛋白在各组中的表达。结果 实验组SGC的TUNEL染色明显增强,免疫组化检测实验组Caspase-12蛋白含量在噪声刺激后迅速增高,1、4 d达到高峰.14 d减少。结论 强噪声可以诱导SGC凋亡,Caspase-12活化引起内质网应激反应性凋亡通道是此过程的信号途径之一。更多还原

【Abstract】 Objective To explore whether intense noise can induce sprial ganglion cell(SGC) apoptosis in guinea pigs,and observe the effects of Caspase- 12 in intense noise- induced cochlea SGC injury.Methods 20healthy white male guinea pigs were selected and exposed to 4 k Hz narrow band noise 120 dB SPL for 4 h.They were assigned to 1 d,4 d and 14 d after noise simulation groups and control group with 5 in each group.Auditory brainstem response was tested in all the groups before put to death.SGC apoptosis was tested by terminal- deoxynucleotidyl transferase mediated nick end labeling(TUNEL)and transmission electron microscopy.Expression of Caspase- 12 was tested by immunohistochemical method.Results TUNEL staining of SGC significantly enhanced in experimental group.Caspase- 12 content increased rapidly after noise simulation,peak times of which were day 1 and day 4,and decreased in day 14.Conclusion Intense noise can induce SGC apoptosis.The activation of Caspase- 12 induces endoplasmic reticulum stress reactivity apoptosis channel,which is one of signal pathways of this process.更多还原