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腺三酸盐对大鼠氧化中毒性的保护作用
Ertugrul Erhan1, Zeynep Suleyman2, Durdu Altuner3
1Department of Otorhinolaryngology, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, Türkiye.
Scientific reports
|November 6, 2025
概括
腺三酸盐 (ATP) 减轻了在老鼠中氧化 (HCQ) 诱导的耳毒性. ATP保护前庭耳神经组织免受氧化损伤,并减少HCQ引起的组织病理变化.
科学领域:
- 耳毒性研究研究
- 神经科学是一个神经科学.
- 药理学 药理学是指药理学的学科.
背景情况:
- 已知氧化 (HCQ) 会引起耳毒性.
- 氧化应激在HCQ诱导的耳毒性中起作用.
- 腺三酸盐 (ATP) 具有潜在的保护性质.
研究的目的:
- 在大鼠模型中研究ATP对HCQ诱导的耳毒性产生保护作用.
- 为了评估ATP在HCQ给药后在前庭耳神经中对氧化应激标志物的影响.
主要方法:
- 24只雄性Wistar大鼠被分为四组:对照组,单独使用ATP,单独使用HCQ和ATP+HCQ.
- 鼠每天接受10天内内注射ATP (4mg/kg) 或盐水.
- HCQ (120 mg/kg) 在ATP/盐水后1小时口服.
- 静脉耳神经组织分析了氧化剂/抗氧化剂参数和组织病理学变化.
主要成果:
- ATP显著抑制了前庭耳神经组织中HCQ诱导的马隆迪甲 (MDA) 的增加.
- ATP减弱了由HCQ引起的抗氧化剂水平 (谷氨,超氧化物脱酶,催化酶) 的下降.
- 组织病理学检查显示,ATP减少了HCQ治疗的老鼠的胀,血管拥堵和原沉积.
结论:
- ATP显示出对氧化诱导的耳毒性有显著的保护作用.
- ATP可以缓解前列耳神经的氧化损伤和相关的组织病理变化.
- ATP可能是预防或减少HCQ相关听力损伤的潜在治疗剂.
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