新巴瓦伊索弗拉通过ALOX15/PGC1-α轴保护H9c2细胞免受H2O诱导的线粒体功能障碍
Linyue Dong1, Yue Zhou1, Liyun Wang2,3
1Department of TCM Chemistry, School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Journal of biochemical and molecular toxicology
|November 1, 2024
概括
新巴瓦伊索弗拉 (NBIF) 通过减少脂质过氧化和改善线粒体功能来保护心脏细胞免受氧化损伤. 通过ALOX15/PGC-1α通路,NBIF对过氧化 (H2O2) 引起的心肌损伤进行屏蔽.
科学领域:
- 心血管生物学 心血管生物学
- 氧化压力研究研究 氧化压力研究
- 自然产品药理学 自然产品药理学
背景情况:
- 氧化应激是心肌损伤的一个关键因素.
- 过氧化 (H2O2) 是心肌细胞中氧化应激的常见诱导剂.
- 天然抗氧化剂为心脏病提供潜在的治疗益处.
研究的目的:
- 研究Neobavaisoflavone (NBIF) 对H9c2心肌细胞中H2O2诱导的氧化应激的保护作用.
- 阐明潜在的分子机制,重点关注线粒体功能和特定的信号通路.
主要方法:
- H9c2细胞暴露在H2O2中,有或没有NBIF处理.
- 用细胞计数工具-8.8评估细胞活力.
- 测量了线粒体膜潜力,脂质基,12-和15-基酸酸 (HETE),ALOX15,PGC-1α和caspase-3等.
主要成果:
- 在H9c2细胞中,H2O2诱导了显著的脂质过氧化,线粒体功能障碍和亡.
- NBIF治疗逆转了这些效应,减少了脂质基,恢复了线粒体膜的潜力.
- NBIF降低了ALOX15表达和12-和15-HETE的产生,同时上调了PGC-1α和Nrf1,从而抑制了caspase-3的激活.
结论:
- NBIF证明了对H2O2诱导的氧化损伤的显著心脏保护作用.
- 保护机制涉及ALOX15途径的抑制和通过PGC-1α增强线粒体生物发生.
- NBIF代表了一种有前途的治疗药物,可以缓解与氧化应激有关的心肌损伤.
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