洛森胺通过SIRT3/Foxo3信号通路减弱ROS介导的血管内皮原生细胞损伤和线粒体功能障碍

Junfang Yuan¹, Yuzhong Wang², Defeng Wang¹

¹Department of Endocrinology, Affiliated Hospital of Hebei University of Engineering, Handan, Hebei Province, People's Republic of China.

Journal of biochemical and molecular toxicology

|July 7, 2023

概括

洛克塞纳提德通过减少氧化应激和亡来保护内皮原生细胞免受高葡萄糖损伤. 这种作用涉及激活SIRT3/Foxo3通路,为糖尿病血管并发症提供潜在的治疗点.

科学领域:

内分泌学和新陈代谢学
血管生物学血管生物学
细胞生物学细胞生物学

背景情况:

糖尿病 (DM) 是一个与内皮原生细胞 (EPC) 功能障碍相关的全球健康危机.
在糖尿病患者中,EPC功能障碍导致血管并发症.
在糖尿病的背景下,Loxenatide对EPC的治疗潜力在很大程度上尚未被探索.

研究的目的:

为了研究洛克森胺对高葡萄糖诱导的功能障碍和EPC中的亡的影响.
阐明潜在的分子机制,包括氧化应激和线粒体通路的作用.
探索SIRT3/Foxo3信号通路的参与.

主要方法:

EPCs的隔离和特征.
用洛克森和高葡萄糖治疗EPC.
定量实时PCR和西布洛特用于基因和蛋白质表达分析.
流式细胞计量和细胞计数套件-8测定细胞亡和细胞活力.
海马XFp分析用于线粒体呼吸和线粒体膜潜力 (MMP) 试验.

主要成果:

洛森胺显著减弱了高葡萄糖诱导的活性氧物种 (ROS) 生产和EPCs中的线粒体依赖性亡.
洛森胺治疗抑制了高葡萄糖诱导的线粒体呼吸功能障碍.
这些保护作用是通过激活sirtuin 3 (SIRT3) / Foxo3信号通路来实现的.

结论:

洛克萨纳提德在EPC中显示出对高葡萄糖诱导的亡的保护作用.
该机制涉及通过SIRT3/Foxo3通路调节ROS生产和线粒体功能.
洛克萨纳提德是减轻糖尿病血管并发症的有希望的治疗候选者,它通过保护EPC功能来减轻糖尿病血管并发症.

关键词:

通过SIRT3/Foxo3信号通路传递信息.在糖尿病中,糖尿病是血糖类的.洛克塞纳提德 (loxenatide) 是一种类型的线粒体中的线粒体.

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