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1-(N-乙酰基-6-氨基己基)-3-羟基-2-甲基吡啶-4-酮与绿茶提取物联合对神经母细胞瘤(SH-SY5Y)细胞铁诱导的氧化损伤的保护作用

Protection of Iron-Induced Oxidative Damage in Neuroblastoma (SH-SY5Y) Cells by Combination of 1-(N-Acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one and Green Tea Extract.

作者信息

Chansiw Nittaya, Kulprachakarn Kanokwan, Paradee Narisara, Prommaban Adchara, Srichairatanakool Somdet

机构信息

School of Medicine, Mae Fah Luang University, Chiang Rai 57100, Thailand.

Research Institute for Health Science, Chiang Mai University, Chiang Mai 50200, Thailand.

出版信息

Bioinorg Chem Appl. 2021 Apr 20;2021:5539666. doi: 10.1155/2021/5539666. eCollection 2021.

DOI:10.1155/2021/5539666
PMID:33986790
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8079199/
Abstract

Iron is a crucial trace element and essential for many cellular processes; however, excessive iron accumulation can induce oxidative stress and cell damage. Neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease, have been associated with altered iron homoeostasis causing altered iron distribution and accumulation in brain tissue. This study aims to investigate the protective effect of 1-(acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one (CM1) in combination with green tea extract (GTE) on iron-induced oxidative stress in neuroblastoma (SH-SY5Y) cells. Cells were cultured in medium with or without ferric chloride loading. Their viability and mitochondrial activity were assessed using MTT and JC-1 staining methods. Levels of the cellular labile iron pool (LIP), reactive oxygen species (ROS), and lipid-peroxidation products were determined using calcein acetoxymethyl ester, 2',7'-dichlorohydrofluorescein diacetate, and TBARS-based assays, respectively. The viability of iron-loaded cells was found to be significantly increased after treatment with CM1 (10 M) for 24 h. CM1 co-treatment with GTE resulted in a greater protective effect than their monotherapy. Combination of CM1 and GTE also reduced mitochondrial disruption and LIP content and ROS and TBARS production. In conclusion, the combination of CM1 and GTE exhibits protection against iron-induced oxidative stress in neuroblastoma cells.

摘要

铁是一种关键的微量元素，对许多细胞过程至关重要；然而，铁的过度积累会诱导氧化应激和细胞损伤。神经退行性疾病，如阿尔茨海默病和帕金森病，与铁稳态改变有关，导致脑组织中铁分布和积累的改变。本研究旨在探讨1-(乙酰基-6-氨基己基)-3-羟基-2-甲基吡啶-4-酮(CM1)与绿茶提取物(GTE)联合应用对神经母细胞瘤(SH-SY5Y)细胞中铁诱导的氧化应激的保护作用。细胞在含或不含氯化铁负载量的培养基中培养。使用MTT和JC-1染色方法评估其活力和线粒体活性。分别使用钙黄绿素乙酰氧基甲酯、2',7'-二氯二氢荧光素二乙酸酯和基于硫代巴比妥酸反应物的检测方法测定细胞不稳定铁池(LIP)、活性氧(ROS)和脂质过氧化产物的水平。发现用CM1(10μM)处理24小时后，铁负载细胞的活力显著增加。CM1与GTE联合治疗比单一治疗具有更大的保护作用。CM1和GTE的联合应用还减少了线粒体破坏、LIP含量以及ROS和硫代巴比妥酸反应物的产生。总之，CM1和GTE的联合应用对神经母细胞瘤细胞中铁诱导的氧化应激具有保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f0c/8079199/d8e07c317eb6/BCA2021-5539666.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f0c/8079199/164068d68bf5/BCA2021-5539666.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f0c/8079199/c850bbbe2a92/BCA2021-5539666.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f0c/8079199/bbad6dae8334/BCA2021-5539666.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f0c/8079199/171d184804df/BCA2021-5539666.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f0c/8079199/d8e07c317eb6/BCA2021-5539666.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f0c/8079199/164068d68bf5/BCA2021-5539666.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f0c/8079199/c850bbbe2a92/BCA2021-5539666.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f0c/8079199/bbad6dae8334/BCA2021-5539666.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f0c/8079199/171d184804df/BCA2021-5539666.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f0c/8079199/d8e07c317eb6/BCA2021-5539666.005.jpg

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