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4-octyl itaconate减轻了西斯丁诱导的铁亡,可能是通过激活NRF2/HO-1信号通路

Li Zhang¹, Wenao Song², Hua Li³

¹Department of Laboratory Medicine, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.

Journal of cellular and molecular medicine

|March 20, 2024

概括

4-Octyl itaconate (4-OI) 通过抑制铁亡,可以防止西斯胺诱导的耳毒性. 这种化合物激活NRF2/HO-1通路,减少活性氧物种和炎症,从而保持听觉细胞功能.

科学领域:

耳毒性研究研究
药物诱导损伤的细胞机制
生物医学科学生物医学科学

背景情况:

西斯普拉丁化疗可能会导致耳毒性,导致听力损失.
铁,一种依赖于铁的细胞死亡,与西斯普拉丁诱导的听觉细胞损伤有关.
4-八基伊塔科纳酸 (4-OI) 具有抗炎和抗氧化特性.

研究的目的:

为了研究4-OI在听觉细胞中对西斯普拉丁诱导的铁亡的保护作用.
阐明4-OI作用的潜在分子机制.

主要方法:

细胞活力测试 (CCK8) 和细胞存活的免疫光.
听觉脑干响应 (ABR) 听力测量以评估听力值.
测量反应性氧物种 (ROS),炎症性细胞因子和与铁亡有关的因素.
网络药理学和RNA测序用于机械洞察力.
对NRF2/HO-1信号通路激活的分析.

主要成果:

西斯普拉丁诱导显著的ROS,炎症和铁亡,同时降低NRF2表达.
4-OI 预处理表明具有抗炎和抗氧化作用.
4-OI减轻了西斯胺诱导的细胞损失和保护了耳毛细胞.
4-OI治疗在小鼠中保持了听力值.

结论:

4-OI有效地抑制了听觉细胞中西斯普拉丁诱导的铁亡.
保护机制涉及NRF2/HO-1信号通路的激活.
4-OI 呈现了一个潜在的治疗策略,用于预防西斯普拉丁诱导的听力损失.

关键词:

4 - 八甲基伊塔科纳酸 4-octyl 伊塔科纳酸这就是NRF2的NRF2.西斯普拉丁 (cisplatin) 是一种制剂.铁性化 (ferroptosis) 是一种耳毒性耳毒性耳毒性

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