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低剂量辐射可以通过减少氧化应激和保护线粒体功能来改善多克索鲁比诱导的损伤
Mengmeng Chen1,2, Kang He1, Kai Wang1
1Department of Rehabilitation, School of Nursing, Jilin University, Changchun, China.
PloS one
|February 11, 2025
概括
低剂量辐射 (LDR) 预处理通过减少氧化应激和维护线粒体功能来防止多克索鲁比 (DOX) 诱导的毒性. 这种组合疗法显示出减轻化疗相关损伤的前景.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 在瘤学瘤学.
- 辐射瘤学 辐射瘤学
背景情况:
- 多克索鲁比 (DOX) 是一种重要的化疗剂,但由于严重的毒性,其使用受到限制.
- 低剂量辐射 (LDR) 具有抗炎和免疫调节性质,表明对药物诱导的损伤有潜在的保护作用.
研究的目的:
- 在小鼠模型中研究LDR对DOX诱导的毒性的保护作用.
- 阐明涉及LDR介导脏保护的潜在分子机制.
主要方法:
- 小鼠被分配到对照,LDR,DOX或组合 (COM) 组.
- 毒性是由DOX诱导的;LDR是在72小时前给予的.
- 进行了组织学,免疫组织化学,免疫光和西部斑点分析.
主要成果:
- 与DOX组相比,COM组的血清UREA,UA,Bax和caspase9水平显著降低.
- 在COM组中,MDA水平较低,而Nrf2表达变化较大.
- 线粒体复合体I活性,ATP,NDUFA1和CYC1水平在COM组中得到了增强.
结论:
- 通过减少氧化应激和增强抗氧化活性,LDR预处理减轻了DOX诱导的毒性.
- 激活Nrf2/HO-1/NQO1通路并保护线粒体呼吸链功能.
- LDR展示了作为一种安全有效的策略来抑制DOX诱导的毒性的潜力.
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