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马格诺洛尔通过通过p38 MAPK-FoxO1轴减轻氧化应激,炎症和线粒体功能障碍来减轻超脂血症诱导的内皮疾病

Yezi Zheng¹, Danyu Cheng², Xiaoyu Wang³

¹Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China.

Free radical biology & medicine

|January 9, 2026

概括

马格诺洛 (MAG) 通过减少炎症和氧化应激,有效地治疗高脂血症引起的内皮功能障碍. 它通过p38 MAPK-FoxO1通路起作用,为新的血管并发症疗法提供了潜力.

科学领域:

心血管研究研究心血管研究
分子生物学分子生物学
药理学药理学是指药理学的学科.

背景情况:

内皮功能障碍 (ED) 是心血管疾病的关键因素,通常与高脂血症有关.
马格诺洛尔 (MAG) 来自Magnolia officinalis,具有已知的抗炎和抗氧化特性.

研究的目的:

调查MAG对高脂血症引起的ED的保护作用.
阐明MAG的作用背后的分子机制,重点关注p38 MAPK-FoxO1通路.

主要方法:

实验使用高脂血症模型和人类大动脉内皮细胞 (HAEC) 进行.
使用了转录组分析,FoxO1敲击,p38 MAPK抑制 (SB203580) 和分子对接.
评估ED,炎症,氧化应激和线粒体功能.

主要成果:

在MAG前期治疗显著改善了高脂血症引起的ED,炎症,氧化应激和线粒体功能障碍 in vivo和HAECs.
MAG的保护作用是由p38 MAPK-FoxO1信号通路介导的.
分子对接证实了MAG与FoxO1.1的直接结合.

结论:

MAG在缓解与高脂血症相关的血管内皮功能障碍方面表现出显著的有效性.
这项研究通过p38 MAPK-FoxO1通路阐明了MAG的作用机制,表明了针对血管并发症的基于MAG的治疗方法的潜力.

关键词:

内皮质功能障碍内皮质功能障碍在FoxO1中,FoxO1是FoxO1的第一个代号.炎症炎症是一种炎症.在MAG中,MAG是MAG.线粒体中的线粒体.氧化应激是一种氧化应激.

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