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目的:应用本研究小组建立的内耳拟老化模型,研究其对噪声损伤的敏感性,并探讨线粒体DNA缺失(mtDNA)在大鼠对噪声损伤易感的可能作用。方法:2月龄Wistar大鼠32只随机分为4组,A组每日皮下注射D-半乳糖150mg/kg体重,持续8周;继而暴露于声强为110dBSPL的噪声环境中,每日连续刺激4h,持续2d。B组每日皮下注射0.9%生理盐水150mg/kg体重,持续8周,然后给予噪声暴露,噪声条件同A组。C组用药方法同A组,D组用药方法同B组,C组和D组均不予噪声暴露。造模后2周测试ABR反应阈改变,并测试各组大鼠膜迷路总超氧化物歧化酶活力(T-SOD)、丙二醛(MDA)水平,同时应用巢式PCR(nestPCR)方法检测大鼠膜迷路mtDNA4834缺失突变,并对PCR产物进行测序。结果:A组大鼠ABR反应阈改变[(66.250±6.409)dBSPL]较B组[(35.625±4.955)dBSPL]明显提高,差异有统计学意义(P<0.01)。A组T-SOD显著下降,MDA水平明显提高,与B组差异有统计学意义(P<0.01)。大鼠内耳组织mtDNA4834缺失突变率分别为:A组87.5%(7/8),B组12.5%(1/8),C组75.0%(6/8),D组0(0/8)。结论:内耳拟老化模型大鼠对噪声性聋易感,大鼠内耳组织mtDNA缺失突变可增加模型大鼠对噪声性听力损伤的易感性。
OBJECTIVE: To study the sensitivities of noise-induced damage to the inner ear model established by this research group and to explore the possible role of mitochondrial DNA loss (mtDNA) in susceptibility to noise damage in rats. Methods: Thirty-two 2-month-old Wistar rats were randomly divided into 4 groups. Group A received daily subcutaneous D-galactose 150 mg / kg body weight for 8 weeks and then exposed to a noisy environment with a sound intensity of 110 dB SPL. Stimulation 4h, sustained 2d. In group B, daily 0.9% saline 150mg / kg body weight was injected subcutaneously for 8 weeks and then exposed to noise. The noise conditions were the same as those in group A. Group C was treated in the same way as Group A, Group D was treated with the same method as Group B, Group C and Group D were not exposed to noise. The changes of ABR threshold were tested 2 weeks after the model establishment, and the levels of total superoxide dismutase (T-SOD) and malondialdehyde (MDA) of the rats in each group were measured, and nested PCR (nestPCR) Rat labyrinth mtDNA4834 deletion mutation, and PCR products were sequenced. Results: The threshold of ABR response in group A [(66.250 ± 6.409) dBSPL] was significantly higher than that in group B [(35.625 ± 4.955) dBSPL], the difference was statistically significant (P <0.01). A group of T-SOD decreased significantly, MDA increased significantly, with the difference between the B group was statistically significant (P <0.01). The mutation rates of mtDNA4834 in rat inner ear were 87.5% (7/8) in group A, 12.5% (1/8) in group B, 75.0% (6/8) in group C and 0 (0/8) in group D, respectively. Conclusion: The model of inner ear aging is susceptible to noise-induced deafness. The deletion of mtDNA in rat inner ear tissue may increase the susceptibility to noise-induced hearing impairment in model rats.