酸通过TLR4/NF-κB信号通路减少氧化应激和炎症反应,改善酸诱导的耳损伤
Yi Lin1, Lili Li2, Jianbin Cheng3
1Department of Otolaryngology, Fujian Provincial Geriatric Hospital, Fuzhou, China.
Clinical and experimental pharmacology & physiology
|August 26, 2025
概括
酸 (CGA) 通过减少尾中的氧化应激和炎症来防止酸盐 (SS) 引起的听力损伤. 这项研究表明CGA
科学领域:
- 耳毒性研究
- 药理学
- 神经科学
背景情况:
- 已知酸盐会导致听力损伤和耳.
- 酸 (CGA) 具有抗氧化和抗亡的特性.
- CGA对耳的保护作用仍未得到研究.
研究的目的:
- 调查酸 (CGA) 对酸盐 (SS) 诱导的耳毒性的潜在保护作用.
- 阐明CGA在尾中的保护作用的机制.
主要方法:
- 在使用SS的老鼠中诱导了耳损伤.
- 小鼠接受了不同剂量的CGA (150,300,600 mg/ kg) 治疗.
- 评估了声行为,氧化应激,炎症,耳病理,亡以及TLR4/NF-κB通路.
主要成果:
- 通过听觉脑干反应 (ABR) 和行为测试成功诱导了耳损伤.
- 增加了氧化应激 (ROS,MDA) 和炎症 (TNF-α,IL- 1β) 标志物.
- CGA治疗显著改善了SS诱导的耳损伤,细胞亡和TLR4/NF-κB通路的激活.
结论:
- 酸 (CGA) 有效地减轻由酸盐 (SS) 引起的耳毒性.
- 通过抑制TLR4/NF-κB通路来发挥其保护作用,从而减少氧化应激和炎症.
- 在预防耳损伤和相关听力损伤方面,CGA显得有前途.
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