皮塞坦诺尔通过SIRT3通路抑制自,保护PC-12细胞免受氧化损伤和线粒体功能障碍
Jie Liu1,2, Peishi Mai1, Zihui Yang1
1Key Laboratory of Geriatric Nutrition and Health, Ministry of Education, Beijing Technology and Business University (BTBU), Beijing 100048, China.
Nutrients
|July 14, 2023
概括
皮塞坦诺尔通过改善线粒体功能和通过SIRT3通路抑制自性来保护神经元细胞免受氧化应激. 这种化合物为神经退行性疾病提供了潜在的治疗益处.
科学领域:
- 神经科学是一个神经科学.
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 氧化应激是神经退行性疾病的关键因素.
- 过氧化 (H2O2) 诱导与这些条件相关的细胞损伤.
研究的目的:
- 研究piceatannol对PC-12细胞中H2O2诱导的损伤的保护作用.
- 阐明底层机制,重点关注线粒体功能和自.
主要方法:
- PC-12细胞先用piceatannol进行预处理,然后暴露于H2O2.
- 评估了线粒体功能,活性氧物种 (ROS) 水平和自标志物.
- 使用一种特定的抑制剂 (3-TYP) 和一种自激活剂 (拉帕米辛) 评估了sirtuin 3 (SIRT3) 的作用.
主要成果:
- 皮塞坦诺显著降低了H2O2诱导的PC-12细胞死亡.
- 它增强了线粒体的含量和功能,包括ROS消除和TFAM,PGC-1α和复合物IV的表达.
- 皮塞坦诺尔抑制了自,恢复了线粒体膜潜能,并减少了自细胞标记物 (LC3B II/I,ATG5).
- 皮塞坦诺治疗增加了SIRT3表达;其抑制消除了保护作用并加剧了损伤.
- 自的激活否定了piceatannol的益处.
结论:
- 皮塞坦诺尔在神经元细胞中表现出对抗氧化应激的细胞保护作用.
- 这些好处是由通过SIRT3途径抑制自介导的,从而改善线粒体功能.
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