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甲基尼古丁胺通过SIRT1的过度表达促进与年龄相关的耳损伤

Toru Miwa^1,2, Akihito Tarui^1,2, Teppei Kouga³

¹Department of Otolaryngology, Teikyo University Hospital, Mizonokuchi, Kawasaki, Japan.

Frontiers in cellular neuroscience

|February 17, 2025

概括

补充N-甲基尼古丁胺 (MNAM) 通过扰乱耳代谢并增加SIRT1蛋白水平,加速与年龄相关的听力损失 (ARHL). 这凸显了MNAM对听觉功能和衰老的有害影响.

科学领域:

耳鼻喉科耳鼻喉科耳鼻喉科
衰老研究研究衰老研究
分子生物学分子生物学

背景情况:

与年龄相关的听力损失 (ARHL) 受遗传,衰老和环境因素的影响.
赛尔图因,特别是SIRT1,是衰老和压力反应的关键调节者.
尼古丁胺 N-甲基转移酶 (NNMT) 和其产物 N1-甲基尼古丁胺 (MNAM) 调节SIRT1并影响ARHL.

研究的目的:

研究MNAM补充剂对小鼠SIRT1表达和ARHL的影响.
为了评估听觉功能,耳形态和MNAM管理后的代谢概况.

主要方法:

低脂肪饮食 (LFD) 养的B6和CBA小鼠接受了LFD或LFD + MNAM.
通过听觉脑干反应 (ABR) 和扭曲产物耳声发射 (DPOAE) 来评估听觉功能.
在多个时间点分析了耳组织学,SIRT1表达和代谢概况.

主要成果:

在两种小鼠菌株中,MNAM补充剂加速了ARHL,在B6小鼠中更显著.
观察到升高的ABR值,外皮毛细胞功能障碍和尾细胞细胞数量减少.
MNAM增加了耳SIRT1蛋白水平 (转录后调节),并破坏了线粒体和TCA循环通路.

结论:

由MNAM诱导的SIRT1过度表达会破坏新陈代谢平衡,加速耳衰老.
MNAM对ARHL有不利影响,强调需要精确的SIRT1调制.
针对平衡SIRT1表达的有针对性的策略对于保持听觉功能至关重要.

关键词:

这是一种N1-甲基尼古丁胺胺.在Sirtuin 11中使用.与年龄有关的听力损失.听觉脑干反应的响应.代谢组代谢组的代谢螺旋带带的螺旋带是什么

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