曼吉费林诱导自会保护听觉毛细胞免受耳毒性影响
Gyeong Min Lim1,2, Gwang-Won Cho1,2,3, Chul Ho Jang4,5
1Department of Biological Science, College of Natural Science, Chosun University, 309 Pilmun-Daero, Dong-Gu, Gwangju, 61452, Republic of Korea.
Molecular neurobiology
|February 15, 2025
概括
曼吉费林是一种天然化合物,通过减少氧化应激和促进听觉毛细胞的自来保护听力. 这种化合物在细胞培养和听力损失的动物模型中有效地防止毛细胞退化.
科学领域:
- 耳部毒理学 耳部毒理学
- 细胞生物学 细胞生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 氧化应激是听觉毛细胞损伤和听力损失的主要驱动因素.
- 减少活性氧物种 (ROS) 是保护听觉功能的潜在策略.
- 曼吉费林是一种来自果的类素,正在研究其自身保护的潜力.
研究的目的:
- 调查曼吉费林对抗氧化应激诱导损伤的耳部保护作用.
- 阐明曼吉费林保护作用背后的机制,重点关注自和亡.
- 在体内评估曼吉费林在减轻耳毒性方面的疗效.
主要方法:
- 在体外研究中,使用暴露于过氧化 (H2O2) 的HEI-OC1细胞进行了实验.
- 对与自相关的蛋白质 (LC3,SQSTM1) 和亡标记物的分析.
- 在试验猪和老鼠的体内研究,使用kanamycin/furosemide诱导的耳毒性模型.
- 听觉脑干反应 (ABR) 测试,扫描电子显微镜 (SEM) 和免疫组织化学.
主要成果:
- 曼吉费林保护HEI-OC1细胞免受H2O2诱导的氧化应激,通过调节自和减少ROS.
- 曼吉费林治疗导致LC3转化和SQSTM1降解,表明自细胞激活.
- 在体内,mangiferin显著降低了Corti器官中的毛细胞退化,并保留了带状突触.
- 曼吉费林在细胞培养和动物模型中都显示出自身保护作用.
结论:
- 曼吉费林对抗氧化应激和耳毒性具有显著的耳保护性.
- 保护机制包括诱导自和消除ROS.
- 曼吉费林作为预防听力损失的治疗剂具有前景.
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