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目的:探讨噪声习服对听觉损伤的保护作用机制。方法:建立噪声习服实验动物模型。采用免疫组织化学、激光扫描共聚焦显微镜(LSCM)及图像分析等技术,定量研究噪声习服后毛细胞内纤维状肌动蛋白(F-actin)、钙调蛋白(CaM)、热休克蛋白70(HSP70)的表达及游离Ca2+浓度的变化。结果:噪声暴露后毛细胞中F-actin、CaM及HSP70的表达均呈增加趋势。与噪声损伤暴露组(H组)比较,噪声习服后损伤暴露组(CH组)中F-actin和HSP70的表达均明显增多,CaM的表达具有增加趋势。声暴露后毛细胞内游离Ca2+浓度升高,噪声损伤暴露组毛细胞内游离Ca2+浓度明显高于噪声习服组(C组)和习服后损伤暴露组。结论:噪声习服使毛细胞对于其后声刺激的保护性反应增强,毛细胞内细胞骨架系统的加强及胞内钙稳态的维持在噪声习服的保护机制中具有重要意义。
Objective: To explore the protective mechanism of noise acclimation on auditory impairment. Methods: To establish a laboratory animal model of noise acclimatization. Immunohistochemistry, laser scanning confocal microscopy (LSCM) and image analysis techniques were used to quantitatively study the expression of F-actin, calmodulin (CaM), heat shock protein 70 (HSP70) expression and free Ca2 + concentration changes. Results: The expression of F-actin, CaM and HSP70 in hair cells increased after noise exposure. Compared with the noise-exposed group (H group), the expression of F-actin and HSP70 in the exposed group (CH group) increased significantly after noise acclimation and the expression of CaM increased. After exposure, the concentration of free Ca2 + in hair cells increased, and the concentration of free Ca2 + in hair cells exposed to noise-induced injury was significantly higher than that in noise-acclimation group (C group) and post-accrual injury group. CONCLUSION: The noise acclimation enhances the protective response of hair cells to the subsequent acoustic stimulation, and the enhancement of the cytoskeleton system in hair cells and the maintenance of intracellular calcium homeostasis are important in the protection mechanism of noise acclimation.