目的探讨噪声暴露前后锰超氧化物歧化酶(Mn-SOD)在大鼠螺旋神经节不同区域表达分布的差异与噪声性聋高频听力易损性的相关性.方法 SD大鼠随机分为两组:实验组给予白噪声115dB 2h 3d造模,不处理者为对照组.ABR测听分析噪声损伤情况;免疫组织化学染色法分析噪声暴露前后Mn-SOD在螺旋神经节不同区域的表达水平;黄嘌呤氧化酶法检测Mn-SOD在螺旋神经节不同区域的活性及变化趋势.结果①ABR:大鼠噪声暴露后与暴露前相比,4、8、16、20、32 kHz ABR阈值均明显上移,以高频听阈变化更为显著;②免疫组织化学染色:在正常情况下,顶部螺旋神经节的Mn-SOD的阳性表达较底部明显;噪声暴露后,Mn-SOD在螺旋神经节的表达较对照组相应部位均显著增高;且顶部较底部的表达增强更为显著;③Mn-SOD活性测定:在正常情况下,顶部螺旋神经节的Mn-SOD活性与底部相比无统计学差异,噪声暴露后,Mn-SOD活性较对照组相应部位均有下降,且底部较顶部更为显著.结论 Mn-SOD在螺旋神经节顶、底部区域的表达分布差异,可能是噪声性聋高频听力易损性的分子机制之一.
Objective To study distribution of Mn-SOD throughout the spiral ganglion and its correlation with the vulnerability of high-frequency hearing to noise induced damage. Methods Rats were divided into an experimental and a control group. The experimental animals were exposed to white noise at 115 dB SPL 2h/day for 3 days. Auditory brainstem responses (ABRs) were used to determine acoustic trauma in experimental animals. Immunohistochemical methods were used to identify the distribution of Mn-SOD in the spiral ganglion, before and after noise exposure. Activity levels of Mn-SOD in different regions of the spiral ganglion were assessd by xanthine oxidase method. Results (1) ABRs:, ABR thresholds at 4, 8, 16,20 and 32 kHz were significantly elevated 3 days after noise exposure, especially in the high-frequency range. (2) Immunohistochemical staining: in normal spiral ganglions, the intensity of Mn-SOD immunoreactivity and numbers of immunopositive neurons appeared to be greater at the cochlear apex than at the base, with roughly intermediate findings in the middle turn. After noise exposure, the expression of Mn-SOD in the spiral ganglion was significantly higher than normal control group, especially at the apex. (3) Mn-SOD activity:After noise exposure, Mn-SOD activity levels declined compared with the control group, especially in the basal region. Conclusion These findings suggest that spiral ganglion cells response to ROS exposure may vary along the cochlear spiral, and the difference in response capacity between the cochlear apex and base may explain the susceptibility to noise induced high-frequency hearing loss.