皮质醇使耳毛细胞通过内源性亡途径对胺素毒性产生敏感性
概括
压力激素皮质醇,在特定度下,使耳毛细胞对 جنت米辛敏感,增加了亡和氧化应激. 这表明皮质醇可能会恶化氨基糖化物诱导的听力损失.
科学领域:
- 耳毒性研究研究
- 细胞毒理学 细胞毒理学
- 内分泌学 在内分泌学.
背景情况:
- 氨基糖化物是感觉神经听力损失的常见原因.
- 像皮质醇这样的高压激素在接受氨基甘油治疗的患者中很常见.
- 皮质醇对氨基糖化物诱导的耳毛细胞损伤的影响尚不清楚.
研究的目的:
- 为了研究皮质醇预治疗是否会影响耳毛细胞中 gentamicin 诱导的耳毒性.
- 探索皮质醇在aminoglycosideototoxicity中的潜在作用的分子机制.
主要方法:
- 使用的家用耳朵研究所 - 科尔蒂的器官1 (HEI-OC1) 细胞用于实验.
- 在接受皮质醇预处理或不接受皮质醇预处理后,评估细胞活力,细胞亡和氧化应激.
- 通过使用受体抑制剂,研究了葡萄糖皮质体受体 (GR) 和矿物质皮质体受体 (MR) 的作用.
主要成果:
- 皮质醇 (50μmol/l) 预处理使头发细胞对 جنت米辛敏感,增加了亡和氧化应激.
- 皮质醇改变了由 gentamicin 诱导的与亡相关的蛋白质表达.
- 阻断GR或MR可以降低皮质醇介导的对 gentamicin 毒性的敏感性.
结论:
- 皮质醇预处理增强了哺乳动物毛细胞对 gentamicin 毒性的敏感性.
- 这种敏感性涉及内在的亡途径和反应性氧物种的产生.
- 皮质醇可能会加剧aminoglycoside诱导的耳毒性,导致听力损失.
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