阿斯塔ξαν丁通过Nrf2/HO-1通路预防毒性
Faezeh Lorestani1, Ahmad Movahedian1, Adel Mohammadalipour1
1Department of Clinical Biochemistry, Isfahan Pharmaceutical Sciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
Canadian journal of physiology and pharmacology
|September 8, 2023
概括
亚斯丁 (AST) 通过减少氧化应激和改善功能标志物,防止甲基 (MTX) 诱导的损伤. 这种天然的胡卜素调节Nrf2/HO-1通路,为毒性提供了潜在的治疗策略.
科学领域:
- 药理学 药理学是指药理学的学科.
- 毒理学 毒理学 毒理学
- 生物化学 生物化学
背景情况:
- 甲托雷克萨特 (MTX) 是一种已知具有毒性的化疗剂.
- 氧化应激在MTX诱导的毒性中起着至关重要的作用.
- Astaxanthin (AST) 是一种天然的胡卜素,具有抗氧化特性.
研究的目的:
- 在大鼠模型中研究阿斯塔克桑丁 (AST) 对甲醇 (MTX) 诱导的毒性的保护作用.
- 评估AST对氧化应激标志物和Nrf2/HO-1通路在MTX治疗大鼠中的影响.
主要方法:
- 在10天的时间里,雄性Wistar大鼠接受了MTX和不同剂量的AST.
- 通过测量血清肌素,尿素和尿酸水平来评估功能.
- 分析了氧化应激标记物,包括甲 (MDA),超氧化失调酶 (SOD) 和催化酶.
- 研究了Nrf2/HO-1通路的表达.
主要成果:
- 服用MTX导致显著的细胞病理损伤和血清肌素,尿素和尿酸的升高.
- MTX显著增加了组织的MDA水平,并降低了SOD和催化酶活性.
- 根据剂量,AST治疗改善了MTX诱导的功能障碍和氧化应激.
- AST上调了Nrf2/HO-1基因表达和改善了抗氧化酶活动.
结论:
- 阿斯塔丁在老鼠中显示出明显的脏保护作用,防止MTX诱导的毒性.
- AST通过减轻氧化应激和调节Nrf2/HO-1通路来减轻MTX诱导的损伤.
- AST具有作为治疗剂的潜力,可以预防或治疗MTX相关的损伤.
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