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JAK/STAT-IL2轴的药理抑制缓解了西斯产生的耳毒性

Shimei Zheng^1,2, Chang Liu³, Jiahuan Li^1,2

¹ENT Institute and Department of Otorhinolaryngology, Eye & ENT Hospital, Fudan University, 83 Fenyang Road, Shanghai, 200031, China.

Molecular neurobiology

|November 19, 2025

概括

这项研究表明,抑制JAK/STAT通路可以保护听力细胞免受损伤. 一种JAK抑制剂Ifidancitinib降低了西斯普拉丁诱导的耳毒性,并改善了小鼠的听力.

科学领域:

耳毒性研究研究
神经科学是一个神经科学.
药理学药理学是指药理学的学科.

背景情况:

感官神经听力损失 (SNHL) 是一种常见的疾病,由耳毛细胞 (HCs) 的不可逆转损伤引起.
西斯普拉丁诱导的耳毒性是一个重大的临床挑战,导致听力损伤.

研究的目的:

调查JAK/STAT信号通路在西斯普拉丁诱导的耳毒性中所起的作用.
评估ifidancitinib,一个JAK1/JAK3抑制剂,作为预防SNHL的潜在治疗剂.

主要方法:

使用HEI-OC1细胞系进行药物查.
耳扩展器研究,以评估对耳毒性的保护.
在成年小鼠体内研究,使用听觉脑干反应 (ABR) 和形态分析.
西部斑点,MitoSOX红色测定和ELISA分析分子机制.
STRING分析和IL-2抑制/补充以阐明JAK-STAT5-IL2轴.

主要成果:

抑制JAK/STAT通路保护HEI-OC1细胞免受西斯诱导的耳毒性.
伊斐达西尼布在耳扩展器中显示出优异的保护,并在小鼠中改善了ABR值和HC形态.
JAK/STAT信号促进了ROS积累和亡;ifidancitinib降低了前炎性标志物.
保护作用通过JAK/STAT5-IL2轴进行介导.

结论:

JAK/STAT信号通路对毛细胞存活至关重要,并且代表了SNHL的可行的治疗标.
伊斐达西尼布在预防和治疗因耳毒性引起的感觉神经神经听力损失方面表现有前途.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.听力损失听力损失在IL-2中,IL-2被认为是IL-2.炎症反应是一种炎症反应.雅克抑制剂的使用

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