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鱼油对丙烯酰胺诱导的大脑皮质氧化应激和神经元凋亡的改善作用。

Ameliorating effect of fish oil on acrylamide induced oxidative stress and neuronal apoptosis in cerebral cortex.

机构信息

Department of Biochemistry, Cell Biology Laboratory, University of Madras, Guindy Campus, Chennai 600025, Tamil Nadu, India.

出版信息

Neurochem Res. 2012 Sep;37(9):1859-67. doi: 10.1007/s11064-012-0794-1. Epub 2012 May 31.

DOI:10.1007/s11064-012-0794-1
PMID:22648048
Abstract

Acrylamide (ACR) is a known industrial toxic chemical that produce neurotoxicity characterized by progressive neuronal degeneration. This study was designed to investigate the protective effect of fish oil on ACR-induced neuronal damage in Wistar rats. ACR enhances the production of reactive oxygen species and potentially affects brain. ACR administered rats showed increased levels of lipid peroxidative product, protein carbonyl content, hydroxyl radical and hydroperoxide which were significantly modulated by the supplementation of fish oil. The activities of enzymic antioxidants and levels of reduced glutathione were markedly lowered in ACR-induced rats; fish oil treatment augmented these antioxidant levels in cortex. Free radicals generated during ACR administration reduced the activities of membrane adenosine triphosphatases and acetylcholine esterase. Fish oil enhanced the activities of these enzymes near normal level. Histological observation represented the protective role of fish oil in ACR-induced neuronal damage. Fish oil reduced the ACR-induced apoptosis through the modulation in expressions of B-cell lymphoma 2 (Bcl2)-associated X protein and Bcl2-associated death promoter. Further, fish oil increases the expression of heat shock protein 27 (Hsp27) in ACR-induced rats. This study provides evidence for the neuroprotective effect of fish oil on ACR-induced neurotoxicity by reducing oxidative stress and apoptosis with modulation in the expression of Hsp27.

摘要

丙烯酰胺(ACR)是一种已知的工业有毒化学物质,会产生以进行性神经元退化为特征的神经毒性。本研究旨在探讨鱼油对 Wistar 大鼠 ACR 诱导的神经元损伤的保护作用。ACR 会增强活性氧的产生,并可能影响大脑。ACR 给药大鼠的脂质过氧化产物、蛋白质羰基含量、羟基自由基和过氧化物水平升高,而鱼油补充可显著调节这些水平。ACR 诱导大鼠的酶抗氧化剂活性和还原型谷胱甘肽水平明显降低;鱼油处理可增加皮质中的这些抗氧化剂水平。ACR 给药期间产生的自由基降低了膜三磷酸腺苷酶和乙酰胆碱酯酶的活性。鱼油可将这些酶的活性增强至接近正常水平。组织学观察代表了鱼油在 ACR 诱导的神经元损伤中的保护作用。鱼油通过调节 B 细胞淋巴瘤 2(Bcl2)相关 X 蛋白和 Bcl2 相关死亡促进剂的表达,减少了 ACR 诱导的细胞凋亡。此外,鱼油可增加 ACR 诱导大鼠中热休克蛋白 27(Hsp27)的表达。本研究提供了证据,表明鱼油通过减少氧化应激和细胞凋亡,并调节 Hsp27 的表达,对 ACR 诱导的神经毒性具有神经保护作用。

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