低幅高频振动通过 AMPK/mTOR 途径恢复线粒体功能,从而改善高血糖诱导的内皮损伤。

IF 0.6 4区 生物学 Q4 CELL BIOLOGY
Xidan Zhang, Jiyu Sun, Xiting Zhu, Zhenghao Yang, Zhuoli Zhu, Min Zhou, Chen Li, Haiyang Yu, Xueqi Gan
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引用次数: 0

摘要

高血糖引起的内皮细胞功能障碍是糖尿病血管并发症发生的关键和起始因素。低幅高频振动(LMHFV)是一种非侵入性生物物理干预措施。据报道,它对高糖诱导的成骨细胞功能障碍有保护作用,但对糖尿病血管并发症却知之甚少。在这项研究中,我们旨在阐明 LMHFV 对高血糖诱导的内皮功能障碍的作用,并假设其保护作用是通过单磷酸腺苷激活蛋白激酶(AMPK)/哺乳动物雷帕霉素靶标(mTOR)途径发挥的。我们分别在正常或 HG 培养基中培养原代小鼠主动脉内皮细胞(MAECs),然后将其暴露于 LMHFV。管形成、细胞旁通透性试验和主动脉环萌发试验表明,LMHFV处理后,MAECs的高糖损伤功能得到了改善。对 MAECs 进行的细胞内 ROS 生成分析、线粒体复合物 I 活性测定、ATP 测定和线粒体膜电位(MMP)测定以及线粒体 ROS 生成分析表明,LMHFV 负载可恢复高糖环境下的线粒体功能。从机理上讲,Western 印迹分析表明,在 LMHFV 诱导的内皮功能恢复过程中,AMPK 磷酸化被促进,mTOR 被抑制。施用 AMPK 抑制剂化合物 C 后,LMHFV 产生的这些保护作用被逆转。这些发现表明,LMHFV 通过 AMPK/mTOR 信号在高糖诱导的损伤 MAEC 中保护内皮细胞功能和线粒体功能方面发挥了重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Low-magnitude high-frequency vibration ameliorates high glucose-induced endothelial injury by restoring mitochondrial function via AMPK/mTOR pathway.

High glucose-induced dysfunction of endothelial cells is a critical and initiating factor in the genesis of diabetic vascular complications. Low-magnitude high-frequency vibration (LMHFV) is a non-invasive biophysical intervention. It has been reported that it exhibits protective effects on high glucose-induced osteoblast dysfunction, but little was known on diabetic vascular complications. In this work, we aim to clarify the role of LMHFV on high glucose-induced endothelial dysfunction and hypothesized that the protective effects functioned through adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway. We cultured primary murine aortic endothelial cells (MAECs) in normal or HG medium, respectively, before exposing to LMHFV. The tube formation, paracellular permeability assay, and aortic ring sprouting assay showed that the high glucose injured-function of MAECs was improved after LMHFV treatment. The intracellular ROS generation analysis, mitochondrial complex I activities measurement, ATP measurement and mitochondrial membrane potential (MMP), and mitochondrial ROS generation analysis of MAECs indicated that mitochondrial function was restored by LMHFV loading in a high glucose environment. Mechanically, western blot assays showed that AMPK phosphorylation was promoted and mTOR was inhibited in LMHFV-induced endothelial function restoration. After the administration of the AMPK inhibitor, Compound C, these protective effects resulting from LMHFV are reversed. These findings suggest that LMHFV plays a significant role in protecting endothelial cells' function and mitochondrial function in high glucose-induced injured MAECs via AMPK/mTOR signalling.

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来源期刊
Journal of Histotechnology
Journal of Histotechnology 生物-细胞生物学
CiteScore
2.60
自引率
9.10%
发文量
30
审稿时长
>12 weeks
期刊介绍: The official journal of the National Society for Histotechnology, Journal of Histotechnology, aims to advance the understanding of complex biological systems and improve patient care by applying histotechniques to diagnose, prevent and treat diseases. Journal of Histotechnology is concerned with educating practitioners and researchers from diverse disciplines about the methods used to prepare tissues and cell types, from all species, for microscopic examination. This is especially relevant to Histotechnicians. Journal of Histotechnology welcomes research addressing new, improved, or traditional techniques for tissue and cell preparation. This includes review articles, original articles, technical notes, case studies, advances in technology, and letters to editors. Topics may include, but are not limited to, discussion of clinical, veterinary, and research histopathology.
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