抗噪音引起的听力损失的NADH:来自"临时"和"永久"聋的模型的证据
1Senior Department of Otolaryngology Head and Neck Surgery, the 6th Medical Center of Chinese PLA General Hospital Chinese PLA Medical School, 6 Fucheng Road, Beijing, 100048, PR China; State Key Laboratory of Hearing and Balance Science, 28 Fuxing Road, Beijing 100853, PR China; National Clinical Research Center for Otolaryngologic Diseases, 28 Fuxing Road, Beijing 100853, PR China.
在小鼠模型中,NADH预处理通过减少耳损伤和保持听觉通路完整性,有效地防止噪音引起的听力损失. 这一发现为预防听力损伤提供了潜在的治疗策略.
科学领域:
- 耳神经病学 耳神经病学
- 分子生物学分子生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 噪音引起的听力损失 (NIHL) 涉及突触和毛细胞损伤,氧化应激和兴奋毒性是关键因素.
- 目前NIHL的治疗方法有限,强调需要有效的治疗干预措施.
研究的目的:
- 调查尼古丁胺氨酸二核酸 (NADH) 对噪音引起的听力损失 (NIHL) 和噪音引起的隐性听力损失 (NIHHL) 的保护作用.
- 阐明NADH在尾中的保护作用的潜在分子机制.
主要方法:
- 利用CBA/CaJ小鼠模型通过噪音暴露诱导NIHHL和NIHL.
- 在暴露于噪音之前,腹腔内注射了NADH.
- 评估了听觉值,突触完整性,外发细胞 (OHC) 损伤,耳 (Ca2+) 水平,反应性氧物种 (ROS),以及mGluR,P-PKC和NRF2的表达.
主要成果:
- NADH预处理减轻了NIHHL中的临时值变化,并减少了NIHL中的永久值升高.
- 在NIHL小鼠中,NADH减弱了突触和OHC损失,保持了立体细胞完整性.
- NADH降低了耳Ca2+水平,ROS,并调节了mGluR,P-PKC和NRF2通路,促进了抗氧化反应.
结论:
- 在小鼠模型中,NADH预处理表明对NIHHL和NIHL都有显著的保护作用.
- NADH的保护机制包括调节Ca2+信号,氧化应激和激活NRF2抗氧化途径.
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