Chemical Characterization of the Avenanthramide-Rich Extract from Oat and Its Effect on D-Galactose-Induced Oxidative Stress in Mice
文献类型: 外文期刊
作者: Ren, Yi 1 ; Yang, Xiushi 1 ; Niu, Xiwu 2 ; Liu, Sen 4 ; Ren, Guixing 1 ;
作者机构: 1.Chinese Acad Agr Sci, Inst Crop Sci, Beijing 100081, Peoples R China
2.Shanxi Agr Univ, Agron Coll, Taigu 030801, Peoples R China
3.Shanxi Univ, Res Ctr Environm Sci & Engn, Taiyuan 030006, Peoples R China
4.Shanxi Acad Agr Sci, Taiyuan 030031, Peoples R China
关键词: Avenanthramides;D-galactose;oxidative stress;mice
期刊名称:JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY ( 影响因子:5.279; 五年影响因子:5.269 )
ISSN: 0021-8561
年卷期: 2011 年 59 卷 1 期
页码:
收录情况: SCI
摘要: The present study was to characterize the avenanthramide-rich extract (ARE) from oat bran and assess its effect on activity and gene expression of antioxidant enzymes in D-galactose-induced oxidativestressed mice. High-performance liquid chromatography (HPLC) analysis found that ARE had 6.07% N-(3',4'-dihydroxycinnamoyl)-5-hydroxyanthranilic acid (Bc), 4.37% N-(4'-hydroxycinnamoyl)-5-hydroxyanthranilic acid (Bp), and 5.36% N-(4'-hydroxy-3'-methoxycinnamoyl)-5-hydroxyanthranilic acid (Bf). In addition, ARE was also rich in vanillic acid (0.60%), caffeic acid (0.50%), syringic acid (0.54%), p-coumaric acid (0.16%), ferulic acid (0.08%), and sinapic acid (0.03%). Administration of D-galactose markedly lowered not only the activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx) but also the gene expression of manganese superoxide dismutase (SOD), copper zinc SOD, glutathione peroxidase (GPx), and lipoprotein lipase (LPL) mRNA in mice. Administration of ARE significantly reversed the D-galactose-induced oxidative stress by increasing the activity of the antioxidant enzymes and upregulating their gene expression. This was accompanied by a significant decrease in the malondialdehyde (MDA) level in mice given ARE compared to the control. The results demonstrated that ARE possessed the antioxidant activity and was effective against D-galactose-induced oxidative stress.
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