Objectives: This study aimed to explore the molecular mechanism of the protective effects of hydrogen-saturated saline on NIHL. Methods: Guinea pigs were divided into three groups: hydrogen-saturated saline; normal saline; and control. For saline administration, the guinea pigs were given daily abdominal injections 3 d before and 1 h before noise exposure. ABR were tested to examine cochlear physiology changes. The changes of 8-hydroxy-desoxyguanosine (8-HOdG), interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-α (TNF-α), intercellular cell adhesion molecule-1 (ICAM-1) and high mobility group box-1 protein (HMGB1) in the cochlea were also examined. Results: The results showed that pre-treatment with hydrogen-saturated saline could significantly attenuate noise-induced hearing loss. The concentration of 8-HOdG was also significantly decreased in the hydrogen-saturated saline group compared with the normal saline group. After noise exposure, the concentrations of IL-1, IL-6, TNF-α, and ICAM-1 in the cochlea of guinea pigs in the hydrogen-saturated saline group were dramatically reduced compared to those in the normal saline group. The concentrations of HMGB-1 and IL-10 in the hydrogen-saturated saline group were significantly higher than in those in the normal saline group immediately and at 7 d after noise exposure. Conclusions: This study revealed for the first time the protective effects of hydrogen-saturated saline on noise-induced hearing loss (NIHL) are related to both the anti-oxidative activity and anti-inflammatory activity.
目的:本研究旨在探讨氢饱和盐水对NIHL的保护作用的分子机制。 方法:将豚鼠分为三组:氢饱和盐水组、生理盐水组、控制组。豚鼠在噪声暴露之前的3天内每天以及暴露前1小时进行盐水腹部注射。检测ABR以检查耳蜗生理变化。还检查了耳蜗中的8-羟基脱氧鸟苷(8-HOdG)、白细胞介素-1(IL-1)、白细胞介素-6(IL-6)、白细胞介素-10(IL-10)、肿瘤坏死因子-α(TNF-α) )、细胞间粘附分子-1(ICAM-1)和高迁移率组box-1蛋白(HMGB1)的变化。 结果:结果表明, 用氢饱和盐水预处理可显著减弱噪声引起的听力损失。与生理盐水组相比, 饱和盐水组的8-HOdG浓度也显著降低。噪声暴露后, 饱和盐水组豚鼠耳蜗中IL-1、IL-6、TNF-α、ICAM-1的浓度明显低于生理盐水组。噪声暴露后, 饱和盐水组中HMGB-1和IL-10的浓度立即显着高于生理盐水组, 7天以后也同样如此。 结论:本研究首次揭示氢饱和盐水对噪声诱发的听力损失(NIHL)的保护作用与抗氧化活性和抗炎活性有关。