5-HMF通过Nrf2/ARE信号通路减轻瞬时性全脑缺血后纹状体的氧化损伤

Cell Stress and Chaperones Pub Date : 2017-01-01 Epub Date: 2016-11-03 DOI:10.1007/s12192-016-0742-0
Bai-Liu Ya, Hong-Fang Li, Hai-Ying Wang, Fei Wu, Qing Xin, Hong-Ju Cheng, Wen-Juan Li, Na Lin, Zai-Hua Ba, Ru-Juan Zhang, Qian Liu, Ya-Nan Li, Bo Bai, Feng Ge
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引用次数: 0

摘要

最近的研究表明,5-羟甲基-2-糠醛(5-HMF)具有良好的生物效应,其对多种神经系统疾病的神经保护作用已引起关注。我们之前的研究表明,5-羟甲基-2-糠醛治疗可防止永久性全脑缺血。然而,脑缺血损伤的内在机制尚未完全明了。本研究旨在探讨 5-HMF 的神经保护作用,并阐明一过性全局性脑缺血后纹状体中核因子红细胞 2 相关因子 2(Nrf2)/抗氧化反应元件(ARE)信号通路的机制。对C57BL/6小鼠进行双侧颈总动脉闭塞20分钟,再灌注24小时后处死。缺血前 30 分钟和再灌注开始后 5 分钟腹腔注射 5-HMF(12 毫克/千克)或等量的载体。再灌注后24小时,通过神经残疾状态量表、运动活动测试和斜梁行走测试评估神经功能。通过甲酚紫染色和末端脱氧核苷酸转移酶(TdT)介导的dNTP缺口末端标记(TUNEL)染色观察纹状体的组织学损伤。氧化应激通过蛋白质中的羰基和丙二醛(MDA)水平进行评估。基于酶联免疫吸附试验(ELISA)的测量方法用于检测 Nrf2 DNA 结合活性。用 Western 印迹法检测了 Nrf2 及其下游 ARE 通路蛋白的表达,如血红素加氧酶-1、NAD (P)H:醌氧化还原酶 1、谷氨酸-半胱氨酸连接酶催化亚基和谷氨酸-半胱氨酸连接酶调节亚基。结果表明,5-HMF能明显改善神经功能缺损,降低脑含水量,减轻纹状体神经元损伤,降低羰基和MDA水平,激活Nrf2/ARE信号通路。综上所述,这些结果表明,5-HMF 可通过激活 Nrf2/ARE 信号通路,在短暂性脑缺血后发挥显著的抗氧化和神经保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
5-HMF attenuates striatum oxidative damage via Nrf2/ARE signaling pathway following transient global cerebral ischemia.

Recent studies have shown 5-hydroxymethyl-2-furfural (5-HMF) has favorable biological effects, and its neuroprotection in a variety of neurological diseases has been noted. Our previous study showed that treatment of 5-HMF led to protection against permanent global cerebral ischemia. However, the underlying mechanisms in cerebral ischemic injury are not fully understood. This study was conducted to investigate the neuroprotective effect of 5-HMF and elucidate the nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway mechanism in the striatum after transient global cerebral ischemia. C57BL/6 mice were subjected to bilateral common carotid artery occlusion for 20 min and sacrificed 24 h after reperfusion. 5-HMF (12 mg/kg) or an equal volume of vehicle was intraperitoneally injected 30 min before ischemia and 5 min after the onset of reperfusion. At 24 h after reperfusion, neurological function was evaluated by neurological disability status scale, locomotor activity test and inclined beam walking test. Histological injury of the striatum was observed by cresyl violet staining and terminal deoxynucleotidyl transferase (TdT)-mediated dNTP nick end labeling (TUNEL) staining. Oxidative stress was evaluated by the carbonyl groups introduced into proteins, and malondialdehyde (MDA) levels. An enzyme-linked immunosorbent assay (ELISA)-based measurement was used to detect Nrf2 DNA binding activity. Nrf2 and its downstream ARE pathway protein expression such as heme oxygenase-1, NAD (P)H:quinone oxidoreductase 1, glutamate-cysteine ligase catalytic subunit and glutamate-cysteine ligase modulatory subunit were detected by western blot. Our results showed that 5-HMF treatment significantly ameliorated neurological deficits, reduced brain water content, attenuated striatum neuronal damage, decreased the carbonyl groups and MDA levels, and activated Nrf2/ARE signaling pathway. Taken together, these results demonstrated that 5-HMF exerted significant antioxidant and neuroprotective effects following transient cerebral ischemia, possibly through the activation of the Nrf2/ARE signaling pathway.

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