1,8-Cineole通过促进Nrf2通路缓解OGD/R诱导的氧化损伤并恢复线粒体功能
Zhenyi Liu1, Jing Wang1, Xiaofei Jin1
1Hebei Key Laboratory of Chinese Medicine Research on Cardio-Cerebrovascular Disease, Hebei University of Chinese Medicine.
Biological & pharmaceutical bulletin
|August 2, 2023
概括
1,8-烯有效降低氧化应激,并恢复细胞中的线粒体功能. 这种化合物激活Nrf2通路,对缺氧-葡萄糖/重氧化损伤提供保护作用.
科学领域:
- 神经保护是一种神经保护.
- 细胞生物学 细胞生物学
- 氧化压力研究研究 氧化压力研究
背景情况:
- 缺氧-葡萄糖和再氧化 (OGD/R) 在HT22细胞中诱导显著的氧化应激损伤和线粒体功能障碍.
- 核因子红色素2相关因子2 (Nrf2) 途径是细胞防御氧化应激的关键调节者.
研究的目的:
- 为了研究1,8-cineole对HT22细胞的OGD/R诱导损伤的保护作用.
- 阐明Nrf2通路在介导1,8-cineole的保护作用中的作用.
主要方法:
- 使用细胞形态,存活率和LDH泄漏,选最佳的1,8-cineole度.
- 对氧化损伤标记物的评估 (SOD,GSH-PX,CAT,ROS,GSH,蛋白碳基,MDA,LPO,8-OHDG).
- 评估线粒体功能 (MMP,ATPase活动) 和Nrf2通路激活 (总Nrf2,核Nrf2,NQO1,HO-1 mRNA和蛋白质水平).
主要成果:
- 10μmol/L的1,8-烯被确定为减轻OGD/R损伤的最佳度.
- 1,8-烯治疗显著增加了抗氧化酶活性和GSH水平,同时降低了氧化应激标志物.
- 1,8-cineole恢复了线粒体膜潜力和ATPase活性,并促进了Nrf2转移到核中,上调NQO1和HO-1表达.
结论:
- 1,8-烯醇有效地减轻HT22细胞中OGD/R诱导的氧化损伤.
- 保护机制涉及Nrf2信号通路的激活.
- 1,8-烯显示出作为一种治疗剂的潜力,用于涉及氧化应激和线粒体功能障碍的条件.
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