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白藜芦醇通过 Drp1/Parkin/PINK1 信号改善衰老样心肌细胞中的线粒体伸长。

Resveratrol Ameliorates Mitochondrial Elongation via Drp1/Parkin/PINK1 Signaling in Senescent-Like Cardiomyocytes.

机构信息

State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau.

Faculty of Chinese Medicine, Macau University of Science and Technology, Taipa, Macau.

出版信息

Oxid Med Cell Longev. 2017;2017:4175353. doi: 10.1155/2017/4175353. Epub 2017 Oct 22.

DOI:10.1155/2017/4175353
PMID:29201272
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5671746/
Abstract

Resveratrol is widely known for its antiaging properties and exerts cardiovascular protective effects in different experimental models. The role of resveratrol in regulating mitochondrial functions and dynamics during the cardiac aging process remains poorly understood. In this study, the effects of resveratrol on mitochondrial morphology and mitochondrial depolarization and on expressions of Drp1, parkin, PINK1, and LC3 were investigated in H9c2 cells after D-galactose treatment that induced senescent-like cardiomyocytes. The results show that downregulation of Drp1 markedly increased mitochondrial elongation. Senescent-like cardiomyocytes were more resistant to CCCP-induced mitochondrial depolarization, which was accompanied by suppressed expression of parkin, PINK1, and LC3-II. Resveratrol treatment significantly increased Drp1 expression, ameliorated mitochondrial elongation, and increased the mitochondrial translocations of parkin and PINK1. In addition, resveratrol significantly enhanced LC3-II expression and decreased TOM20-labeled mitochondrial content. Resveratrol also suppressed the phosphorylation of parkin and PINK1, which may relate to its abilities to degrade the impaired mitochondria in senescent-like cardiomyocytes. These findings show that suppressing mitochondrial elongation in a Drp1-dependent manner is involved in the effect of resveratrol on attenuating the development of aging cardiomyocytes. Activation of parkin and PINK1 may be a potential mechanism of resveratrol for treating cardiovascular complications related to aging.

摘要

白藜芦醇因其抗衰老特性而广为人知，并在不同的实验模型中发挥心血管保护作用。白藜芦醇在调节心脏衰老过程中线粒体功能和动力学中的作用仍知之甚少。在这项研究中，研究了白藜芦醇在 D-半乳糖处理诱导的衰老样心肌细胞后对 H9c2 细胞中线粒体形态和线粒体去极化以及 Drp1、parkin、PINK1 和 LC3 表达的影响。结果表明，下调 Drp1 可显著增加线粒体的伸长。衰老样心肌细胞对 CCCP 诱导的线粒体去极化的抵抗力更强，同时 parkin、PINK1 和 LC3-II 的表达受到抑制。白藜芦醇处理显著增加了 Drp1 的表达，改善了线粒体的伸长，并增加了 parkin 和 PINK1 的线粒体易位。此外，白藜芦醇显著增强了 LC3-II 的表达并减少了 TOM20 标记的线粒体含量。白藜芦醇还抑制了 parkin 和 PINK1 的磷酸化，这可能与其在衰老样心肌细胞中降解受损线粒体的能力有关。这些发现表明，以 Drp1 依赖性方式抑制线粒体伸长参与了白藜芦醇减轻衰老心肌细胞发展的作用。激活 parkin 和 PINK1 可能是白藜芦醇治疗与衰老相关的心血管并发症的潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d493/5671746/73a536356e22/OMCL2017-4175353.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d493/5671746/8a36a97849fb/OMCL2017-4175353.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d493/5671746/73a536356e22/OMCL2017-4175353.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d493/5671746/8a36a97849fb/OMCL2017-4175353.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d493/5671746/58ac1ae7a9fd/OMCL2017-4175353.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d493/5671746/988162168773/OMCL2017-4175353.003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d493/5671746/73a536356e22/OMCL2017-4175353.008.jpg

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