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α-生育酚琥珀酸酯对吲哚美辛诱导的C6胶质瘤细胞分子损伤的影响。

Effect of α-tocopheryl succinate on the molecular damage induced by indomethacin in C6 glioma cells.

作者信息

Pekmez Murat, Önay-Uçar Evren, Arda Nazli

机构信息

Department of Molecular Biology and Genetics, Faculty of Science, Istanbul University, Istanbul 34134, Turkey.

出版信息

Exp Ther Med. 2015 Feb;9(2):585-590. doi: 10.3892/etm.2014.2101. Epub 2014 Dec 3.

DOI:10.3892/etm.2014.2101
PMID:25574239
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4280948/
Abstract

Indomethacin is a member of the non-steroidal anti-inflammatory drug (NSAID) class, which has great potential for use in the treatment of glioma. However, it induces the generation of reactive oxygen species (ROS) and causes molecular damage while inducing its effects. Vitamin E is widely used in the complementary therapy of cancers. The main goal of the present study was to investigate the effects of α-tocopheryl succinate (α-TOS) against the oxidative damage induced by indomethacin in C6 glioma cells. Cells were treated with 10 μM α-TOS alone or in combination with 200 μM indomethacin for two days. The intracellular ROS level, molecular damage as revealed by lipid peroxidation and protein carbonyl formation, and the COX activity in C6 glioma cells were measured. Treatment of the cells with α-TOS and indomethacin, alone or in combination, caused the levels of ROS generation and protein damage to increase, but protected against lipid peroxidation and reduced COX activity.

摘要

吲哚美辛是非甾体抗炎药(NSAID)类的一种,在治疗神经胶质瘤方面具有巨大的应用潜力。然而,它在发挥作用时会诱导活性氧(ROS)的产生并造成分子损伤。维生素E广泛用于癌症的辅助治疗。本研究的主要目的是研究琥珀酸α-生育酚(α-TOS)对吲哚美辛诱导的C6胶质瘤细胞氧化损伤的影响。细胞分别用10μMα-TOS单独处理或与200μM吲哚美辛联合处理两天。测量C6胶质瘤细胞内的ROS水平、脂质过氧化和蛋白质羰基形成所揭示的分子损伤以及COX活性。单独或联合用α-TOS和吲哚美辛处理细胞,会使ROS生成水平和蛋白质损伤增加,但能防止脂质过氧化并降低COX活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f47/4280948/c14f430f61ce/ETM-09-02-0585-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f47/4280948/5712cf36dcec/ETM-09-02-0585-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f47/4280948/3f78222a23ca/ETM-09-02-0585-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f47/4280948/c14f430f61ce/ETM-09-02-0585-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f47/4280948/5712cf36dcec/ETM-09-02-0585-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f47/4280948/3f78222a23ca/ETM-09-02-0585-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f47/4280948/c14f430f61ce/ETM-09-02-0585-g02.jpg

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Bioorg Med Chem Lett. 2010 Sep 1;20(17):5262-8. doi: 10.1016/j.bmcl.2010.06.144. Epub 2010 Jul 23.
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Lancet Oncol. 2009 May;10(5):501-7. doi: 10.1016/S1470-2045(09)70035-X.
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Evolution of nonsteroidal anti-inflammatory drugs (NSAIDs): cyclooxygenase (COX) inhibition and beyond.
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J Biol Chem. 2009 Jan 30;284(5):3058-3068. doi: 10.1074/jbc.M805329200. Epub 2008 Dec 2.
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