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需要P2X7受体用于aminoglycoside在发育中的耳毛细胞中引起的耳毒性
Cheng Cheng1, Jiaoyao Ma2, Xiaoling Lu2
1Department of Otolaryngology Head and Neck Surgery, Affiliated Drum Tower Hospital of Nanjing University Medical School, Jiangsu Provincial Key Medical Discipline (Laboratory), No.321 Zhongshan Road,Nanjing 210008, China.
Neurobiology of disease
|June 1, 2023
概括
氨基甘油酸抗生素 (AGAs) 通过进入耳毛细胞 (HCs) 引起听力损失. 阻止P2X7受体可以防止AGA进入,保护HC免受损伤,并建议预防听力损失的治疗目标.
科学领域:
- 耳毒性研究研究
- 分子生物学分子生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 氨基甘油酸抗生素 (AGAs) 对于治疗严重感染至关重要,但可能导致不可逆转的听力损失.
- AGAs在耳毛细胞 (HCs) 中积累,导致细胞损伤和听觉功能障碍.
- 尼奥米辛治疗增加了HCs的细胞内ATP和P2X7受体表达.
研究的目的:
- 研究P2X7受体在氨基糖化抗生素 (AGA) 吸收和耳毒性中的作用.
- 为了确定P2X7受体缺陷是否能保护耳毛细胞免受AGA诱导的损伤.
- 确定P2X7受体作为预防AGA诱导的听力损失的潜在治疗标.
主要方法:
- 使用了缺乏P2X7受体 (P2rx7-/-) 的转基因淘汰赛小鼠.
- 评估neomycin诱导的毛细胞损伤在体外和体内.
- 在野生类型和P2rx7-/-小鼠中追踪光健美的摄取量.
- 在耳组织中评估了氧化应激和亡的标志物.
主要成果:
- 缺乏P2X7受体显著保护耳毛细胞免受尼奥米诱导的损伤.
- 在野生类型的HC中观察到光健美的吸收,但在P2rx7-/-HC中没有观察到.
- P2rx7淘汰赛抑制了新菌素诱导的线粒体氧化应激和中的亡.
- 听觉功能和HC数量没有被P2rx7缺陷显著改变,因为没有neomycin.
结论:
- P2X7受体促进了氨基糖化抗生素进入耳毛细胞的过程.
- 缺乏P2X7受体可以防止氨基糖化物诱导的耳毒性.
- 向P2X7受体是一个有前途的治疗策略,可以预防与氨基糖化物相关的听力损失.
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