کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8634222 | 1569093 | 2018 | 24 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Up-regulation of HO-1 by Nrf2 activation protects against palmitic acid-induced ROS increase in human neuroblastoma BE(2)-M17 cells
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کلمات کلیدی
PBSnuclear factor erythroid-2-related factor 2p-ERKHeme oxygenase-1N-acetyl-l-cysteineSFADCFH-DAERKHO-1NACNrf2FITC2′,7′-dichlorofluorescein diacetate - 2 '، 7'-dichlorofluorescein diacetateBSA - BSAkeap1 - buy1Phosphorylated ERK - ERK فسفریلیت شدهROS - ROSbovine serum albumin - آلبومین سرم گاوsaturated fatty acid - اسید چرب اشباع شدهsaturated free fatty acids - اسیدهای چرب آزاد اشباع شدهAlzheimer's disease - بیماری آلزایمرNeurological diseases - بیماری های عصبیParkinson's disease - بیماری پارکینسونdihydroethidium - دی هیدروتیدیمendoplasmic reticulum - شبکه آندوپلاسمی antioxidant response elements - عناصر پاسخ آنتی اکسیدانfluorescein isothiocyanate - فلوئورسین ایسوتیوسیاناتPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریARE - هستندheme oxygenase 1 - همای اکسیژناز 1DHE - وPalmitic acid - پالمیتیک اسیدKelch-like ECH-associated protein 1 - پروتئین مرتبط با ECH کلچ 1extracellular-signal-regulated kinase - کیناز تنظیم شده خارج سلولی سیگنالReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
علوم غدد
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چکیده انگلیسی
Saturated fatty acids (SFAs) induce reactive oxygen species (ROS) production in neurons. Extracellular signal regulated kinase (ERK)/nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) is a ROS response pathway. Therefore, high ROS is always accompanied by increase of HO-1, an anti-oxidative enzyme; but it remains unknown why there is no significant reduction of ROS with the increase of HO-1 in SFAs-treated neurons. We hypothesized that the up-regulation of HO-1 is compensatory for response to fatty acid-induced oxidative stress but not enough to reduce ROS levels. We evaluated the anti-ROS effect of HO-1 and the involved pathway in palmitic acid (PA)-treated human neuroblastoma BE(2)-M17 cells. As expected, PA-induced ROS increase was accompanied by activation of the ERK-Nrf2-HO-1 pathway, as demonstrated by an increase in ERK phosphorylation, Nrf2 phosphorylation and nuclear accumulation, and HO-1 expression at the mRNA and protein levels, in a PA-dose-dependent manner. In contrast, administration of the ROS scavenger NAC significantly reduced the levels of PA-regulated ROS and HO-1 protein. However, the ERK inhibitor U0126 not only reversed the activating effect of PA on the ERK-Nrf2-HO-1 pathway but also aggravated PA-induced ROS. Furthermore, the Nrf2-specific activator NK-252 significantly increased PA-up-regulated HO-1 protein and alleviated PA-induced ROS. Therefore, our results suggest that up-regulation of HO-1 in PA-treated neurons is a compensatory response to ROS increase and that increasing HO-1 expression by Nrf2 activation can prevent the process of ROS production in PA-treated neurons.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Nutrition Research - Volume 52, April 2018, Pages 80-86
Journal: Nutrition Research - Volume 52, April 2018, Pages 80-86
نویسندگان
Yun Shi, Yan Sun, Xuepei Sun, Hongye Zhao, Min Yao, Lianguo Hou, Lingling Jiang,