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CD38 与NF-κB协调,以促进噪音引起的听力损失中的耳炎症:阿比基尼尼的保护作用

Da Liu^1,2,3,4,5, Na Sai^1,2,3,4,5, Ying Zhou^1,2,3,4,5

¹Senior Department of Otolaryngology-Head & Neck Surgery, the Sixth Medical Center of PLA General Hospital, Beijing, 100853, China.

Molecular neurobiology

|December 26, 2024

概括

噪音引起的听力损失涉及耳炎症. 通过抑制NF-κB激活,用阿皮基因抑制CD38,从而防止听力损失,这表明CD38是治疗标.

科学领域:

耳鼻喉科耳鼻喉科耳鼻喉科
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

暴露于噪音是感觉神经听力损失的主要原因.
耳炎症,特别是涉及NF-κB信号传递和巨细胞积累,有助于噪音引起的听力损失和毛细胞损伤.
听力损伤后耳炎症的确切机制仍然不完全理解.

研究的目的:

为了研究声学损伤后基底膜中的蛋白质变化.
探索尼古丁胺胺氨基二核酸 (NAD) 代谢和CD38在噪音诱导的耳炎症中的作用.
评估anakinra和apigenin在预防噪音引起的听力损失方面的治疗潜力.

主要方法:

协同质量标记 (TMT) 技术用于分析基底膜中的蛋白质组变化.
动物受到声学伤害以诱导噪音暴露.
药理干预包括给予阿纳金拉 (IL-1受体阻断剂) 和阿皮基宁 (CD38抑制剂).

主要成果:

暴露于噪音导致NAD代谢减少,并激活NF-κB信号通路.
CD38的表达,一个关键的NAD酶,与炎症的发作有关.
通过抑制NF-κB和CD38的表达,阿皮基宁治疗显著降低了听力值的变化,而阿纳金拉显示的效果很小.

结论:

CD38抑制是一种有前途的治疗策略,可以缓解噪音引起的听力损失.
针对CD38/NAD代谢轴可能提供一种新的方法来管理耳炎症.
对NF-κB和CD38通路的进一步研究可能会导致针对听力损伤的有效干预.

关键词:

它们的原生素是apigenin.CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 听力损失听力损失在 NF-κBB 中.

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