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MitoQ 能够调节细胞凋亡和炎症。

MitoQ Is Able to Modulate Apoptosis and Inflammation.

机构信息

Hygiene and Public Health Unit (ASUGI), 34129 Trieste, Italy.

Department of Pediatrics, Institute for Maternal and Child Health-IRCCS Burlo Garofolo, 34137 Trieste, Italy.

出版信息

Int J Mol Sci. 2021 Apr 30;22(9):4753. doi: 10.3390/ijms22094753.

DOI:10.3390/ijms22094753
PMID:33946176
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8124358/
Abstract

Mitoquinone (MitoQ) is a mitochondrial reactive oxygen species scavenger that is characterized by high bioavailability. Prior studies have demonstrated its neuroprotective potential. Indeed, the release of reactive oxygen species due to damage to mitochondrial components plays a pivotal role in the pathogenesis of several neurodegenerative diseases. The present study aimed to examine the impact of the inflammation platform activation on the neuronal cell line (DAOY) treated with specific inflammatory stimuli and whether MitoQ addition can modulate these deregulations. DAOY cells were pre-treated with MitoQ and then stimulated by a blockade of the cholesterol pathway, also called mevalonate pathway, using a statin, mimicking cholesterol deregulation, a common parameter present in some neurodegenerative and autoinflammatory diseases. To verify the role played by MitoQ, we examined the expression of genes involved in the inflammation mechanism and the mitochondrial activity at different time points. In this experimental design, MitoQ showed a protective effect against the blockade of the mevalonate pathway in a short period (12 h) but did not persist for a long time (24 and 48 h). The results obtained highlight the anti-inflammatory properties of MitoQ and open the question about its application as an effective adjuvant for the treatment of the autoinflammatory disease characterized by a cholesterol deregulation pathway that involves mitochondrial homeostasis.

摘要

甲萘醌(MitoQ)是一种具有高生物利用度的线粒体活性氧清除剂。先前的研究表明了它的神经保护潜力。事实上,由于线粒体成分受损而导致的活性氧的释放,在几种神经退行性疾病的发病机制中起着关键作用。本研究旨在研究炎症平台激活对用特定炎症刺激物处理的神经元细胞系(DAOY)的影响,以及添加 MitoQ 是否可以调节这些失调。DAOY 细胞先用 MitoQ 预处理,然后用他汀类药物阻断胆固醇途径(也称为甲羟戊酸途径)刺激,模拟胆固醇失调,胆固醇失调是一些神经退行性和自身炎症性疾病的常见参数。为了验证 MitoQ 所起的作用,我们在不同时间点检查了参与炎症机制和线粒体活性的基因的表达。在这个实验设计中,MitoQ 在短时间(12 小时)内对甲羟戊酸途径的阻断显示出保护作用,但不能长时间持续(24 和 48 小时)。所得结果突出了 MitoQ 的抗炎特性,并提出了将其作为治疗以胆固醇失调途径为特征的自身炎症性疾病的有效辅助剂的应用问题,该疾病涉及线粒体动态平衡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a50/8124358/5df9bc0e63fb/ijms-22-04753-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a50/8124358/fa2eebfa5f69/ijms-22-04753-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a50/8124358/6bb5942c2018/ijms-22-04753-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a50/8124358/614ae2273586/ijms-22-04753-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a50/8124358/5df9bc0e63fb/ijms-22-04753-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a50/8124358/fa2eebfa5f69/ijms-22-04753-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a50/8124358/6bb5942c2018/ijms-22-04753-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a50/8124358/614ae2273586/ijms-22-04753-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a50/8124358/5df9bc0e63fb/ijms-22-04753-g004.jpg

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2
Mitochondrial Oxidative Stress and "Mito-Inflammation": Actors in the Diseases.线粒体氧化应激与“线粒体炎症”:疾病中的作用因素
Biomedicines. 2021 Feb 20;9(2):216. doi: 10.3390/biomedicines9020216.
3
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Endurance training and MitoQ supplementation improve spatial memory, VEGF expression, and neurogenic factors in hippocampal tissue of rats.
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J Clin Transl Res. 2022 Dec 13;9(1):1-7. eCollection 2023 Feb 25.
4
Robust intervention for oxidative stress-induced injury in periodontitis controllably released nanoparticles that regulate the ROS-PINK1-Parkin pathway.针对牙周炎中氧化应激诱导损伤的强效干预措施,可控释放调节ROS-PINK1-Parkin通路的纳米颗粒。
Front Bioeng Biotechnol. 2022 Dec 15;10:1081977. doi: 10.3389/fbioe.2022.1081977. eCollection 2022.
5
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Animals (Basel). 2022 Nov 17;12(22):3181. doi: 10.3390/ani12223181.
6
The Effect of Antioxidant Added to Preservation Solution on the Protection of Kidneys before Transplantation.抗氧化剂添加到保存液中对移植前肾脏保护的影响。
Int J Mol Sci. 2022 Mar 15;23(6):3141. doi: 10.3390/ijms23063141.
Molecules. 2021 Feb 11;26(4):953. doi: 10.3390/molecules26040953.
4
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5
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6
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7
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8
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Front Pharmacol. 2020 Jul 22;11:1034. doi: 10.3389/fphar.2020.01034. eCollection 2020.
9
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Int J Mol Sci. 2020 Jul 1;21(13):4714. doi: 10.3390/ijms21134714.
10
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Front Immunol. 2020 Jun 3;11:947. doi: 10.3389/fimmu.2020.00947. eCollection 2020.