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形态功能分析表明,酪醇可挽救地塞米松诱导的肌肉萎缩。

Morpho-Functional Analyses Demonstrate That Tyrosol Rescues Dexamethasone-Induced Muscle Atrophy.

作者信息

Salucci Sara, Burattini Sabrina, Versari Ilaria, Bavelloni Alberto, Bavelloni Francesco, Curzi Davide, Battistelli Michela, Gobbi Pietro, Faenza Irene

机构信息

Department of Biomedical and NeuroMotor Sciences, University of Bologna, 40126 Bologna, Italy.

Department of Biomolecular Sciences, University of Urbino Carlo Bo, 61029 Urbino, Italy.

出版信息

J Funct Morphol Kinesiol. 2024 Jul 17;9(3):124. doi: 10.3390/jfmk9030124.

DOI:10.3390/jfmk9030124
PMID:39051285
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11270424/
Abstract

Prolonged exposure to high dosages of dexamethasone, which is a synthetic glucocorticoid and a well-known anti-inflammatory drug, may lead to an increase in reactive oxygen species production, contributing to muscle wasting. The prevention of muscle atrophy by ingestion of functional foods is an attractive issue. In the last decade, natural antioxidant compounds have been increasingly investigated as promising molecules able to counteract oxidative-stress-induced muscle atrophy. Recently, we have demonstrated the antioxidant properties of two main olive oil polyphenols also known for their anticancer and anti-inflammatory activities in different cell models. Here, the preventive effect of tyrosol on dexamethasone-induced muscle atrophy has been investigated by means of morpho-functional approaches in C2C12 myotubes. Dexamethasone-treated cells showed a reduced fiber size when compared to control ones. While long and confluent myotubes could be observed in control samples, those exposed to dexamethasone appeared as immature syncytia. Dysfunctional mitochondria and the accumulation of autophagic vacuoles contributed to myotube degeneration and death. Tyrosol administration before glucocorticoid treatment prevented muscle wasting and rescued mitochondrial and lysosomal functionality. These findings demonstrate that tyrosol attenuates dexamethasone-induced myotube damage, and encourage the use of this natural molecule in preclinical and clinical studies and in synergy with other functional foods or physical activity with the aim to prevent muscle atrophy.

摘要

长期暴露于高剂量地塞米松(一种合成糖皮质激素和著名的抗炎药物)可能导致活性氧产生增加,从而导致肌肉萎缩。通过摄入功能性食品来预防肌肉萎缩是一个有吸引力的问题。在过去十年中,天然抗氧化化合物作为有希望对抗氧化应激诱导的肌肉萎缩的分子受到了越来越多的研究。最近,我们已经在不同的细胞模型中证明了两种主要橄榄油多酚的抗氧化特性,它们也以其抗癌和抗炎活性而闻名。在此,通过形态功能方法在C2C12肌管中研究了酪醇对地塞米松诱导的肌肉萎缩的预防作用。与对照细胞相比,地塞米松处理的细胞显示纤维尺寸减小。虽然在对照样品中可以观察到长而融合的肌管,但暴露于地塞米松的肌管表现为不成熟的合胞体。线粒体功能障碍和自噬空泡的积累导致肌管退化和死亡。在糖皮质激素治疗前给予酪醇可预防肌肉萎缩,并挽救线粒体和溶酶体功能。这些发现表明,酪醇可减轻地塞米松诱导的肌管损伤,并鼓励在临床前和临床研究中使用这种天然分子,并与其他功能性食品或体育活动协同使用,以预防肌肉萎缩。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d1/11270424/4839b90913af/jfmk-09-00124-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d1/11270424/67ced1148d2b/jfmk-09-00124-sch001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d1/11270424/93aa2198fa6c/jfmk-09-00124-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d1/11270424/c39b8f9b6370/jfmk-09-00124-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d1/11270424/e75fc1bddfb3/jfmk-09-00124-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d1/11270424/4ee5161a0ccc/jfmk-09-00124-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d1/11270424/4839b90913af/jfmk-09-00124-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d1/11270424/67ced1148d2b/jfmk-09-00124-sch001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d1/11270424/93aa2198fa6c/jfmk-09-00124-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d1/11270424/c39b8f9b6370/jfmk-09-00124-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d1/11270424/e75fc1bddfb3/jfmk-09-00124-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d1/11270424/4ee5161a0ccc/jfmk-09-00124-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d1/11270424/4839b90913af/jfmk-09-00124-g005.jpg

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