Suppr超能文献

生物转化蓝莓汁可保护神经元免受过氧化氢诱导的氧化应激和丝裂原活化蛋白激酶通路改变的影响。

Biotransformed blueberry juice protects neurons from hydrogen peroxide-induced oxidative stress and mitogen-activated protein kinase pathway alterations.

机构信息

Natural Health Products and Metabolic Diseases Laboratory, Department of Pharmacology and Montreal Diabetes Research Center, University of Montreal, PO Box 6128, Downtown Station, Montreal, QC, Canada H3C 3J7.

出版信息

Br J Nutr. 2010 Sep;104(5):656-63. doi: 10.1017/S0007114510001170. Epub 2010 May 12.

Abstract

A growing body of evidence supports the therapeutic effects of blueberry in neurodegenerative disorders. Biotransformation of blueberry juice by Serratia vaccinii bacteria increases its phenolic content and antioxidant activity. In neuronal cell culture, biotransformed blueberry juice (BJ) significantly increased the activity of antioxidant enzymes, namely catalase and superoxide dismutase. Moreover, BJ protected neurons against H2O2-induced cell death in a dose-dependent manner. This associated with the upregulation of mitogen-activated protein kinase (MAPK) family enzymes p38 and c-Jun N-terminal kinase (JNK) activation, as well as with the protection of extracellular signal-regulated kinase (ERK1/2) and MAPK/ERK kinase (MEK1/2) activity loss induced by H2O2. The present studies demonstrate that BJ can protect neurons against oxidative stress possibly by increasing antioxidant enzyme activities and activating p38- and JNK-dependent survival pathways while blocking MEK1/2- and ERK1/2-mediated cell death. Thus, BJ may represent a novel approach to prevent and to treat neurodegenerative disorders, and it may represent a source of novel therapeutic agents against these diseases.

摘要

越来越多的证据支持蓝莓在神经退行性疾病中的治疗作用。经沙雷氏菌(Serratia vaccinii)细菌转化的蓝莓汁增加了其酚类含量和抗氧化活性。在神经元细胞培养中,经生物转化的蓝莓汁(Biotransformed Blueberry Juice,BJ)显著增加了抗氧化酶的活性,如过氧化氢酶和超氧化物歧化酶。此外,BJ 以剂量依赖的方式保护神经元免受 H2O2 诱导的细胞死亡。这与丝裂原激活蛋白激酶(mitogen-activated protein kinase,MAPK)家族酶 p38 和 c-Jun N 末端激酶(c-Jun N-terminal kinase,JNK)的激活以及对 H2O2 诱导的细胞外信号调节激酶(extracellular signal-regulated kinase,ERK1/2)和 MAPK/ERK 激酶(MAPK/ERK kinase,MEK1/2)活性丧失的保护有关。本研究表明,BJ 可以通过增加抗氧化酶的活性和激活 p38 和 JNK 依赖性存活途径来保护神经元免受氧化应激,同时阻断 MEK1/2 和 ERK1/2 介导的细胞死亡。因此,BJ 可能是预防和治疗神经退行性疾病的一种新方法,也可能是针对这些疾病的新型治疗药物的来源。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验