食品科学 ›› 2013, Vol. 34 ›› Issue (3): 29-32.

• 基础研究 • 上一篇    下一篇

6-羟基山萘酚-3-O-β-葡萄糖苷抑制脱氧核糖氧化损伤的机理

王媛凯1,支鹏2,张立伟1   

  1. 1. 山西大学分子科学研究所
    2. 天津大学药物科学与技术学院
  • 收稿日期:2011-12-08 修回日期:2013-01-05 出版日期:2013-02-15 发布日期:2017-12-29
  • 通讯作者: 张立伟 E-mail:lwzhang@sxu.edu.cn
  • 基金资助:
    科技部十二.五“重大新药创制”科技重大专项;山西省回国留学人员科研资助项目基金

The Study of Mechanism of 6-Hydroxykaempferol-3-O-β-glucoside for Inhibiting Oxidative Damage of Deoxyribose

  • Received:2011-12-08 Revised:2013-01-05 Online:2013-02-15 Published:2017-12-29

摘要: 目的:研究6-羟基山萘酚-3-O-β-葡萄糖苷(6-HK-3-O-G)抑制Fenton反应和对羟自由基清除的能力,并对其抑制Fenton反应的机理进行初步探讨。方法:利用脱氧核糖氧化损伤的实验检测模型和DPPH自由基的清除实验。结果:6-HK-3-O-G对羟自由基具有较强的清除能力;对Fenton反应引起的2-脱氧核糖氧化损伤具有保护作用,其保护作用机理与6-HK-3-O-G直接对Fenton反应所产生的羟自由基的清除作用有关,但更主要的可能是由于6-HK-3-O-G 与Fe2+的螯合作用,阻断了Fenton反应的进行。结论:6-HK-3-O-G 具有强的抗氧化活性,在生理条件下,6-HK-3-O-G与Fe2+的络合作用可能是其抑制Fenton反应的关键因素。

Abstract: The Study of Mechanism of 6-Hydroxykaempferol-3-O-β-glucoside for Inhibiting Oxidative Damage of Deoxyribose WANG Yuan-kai1,ZHI peng2,ZHANG Li-wei1,* (1. Institute of Molecular Science, Shanxi University, Taiyuan 030006, China; 2. School of Pharmaceutical Science and Technology,Tianjin University,Tianjin 300072, China) Abstract:Objective:To study the ability of 6-hydroxykaempferol-3-O-β-glucoside(6-HK-3-O-G) for inhibiting Fenton reaction and scavenging hydroxyl radical , and to explore the mechanism of inhibiting the Fenton reaction . Methods: the detection model of deoxyribose oxidative damage and scavenging DPPH?was used . Results 6-HK-3-O -G not only has strong ability of scavenging hydroxyl radical, but also can protect 2-deoxyribose oxidative damage which caused by the Fenton reaction. There are two reasons for 6-HK-3-O-G protecting deoxyribose oxidative damage,one of the reasons is the strong ability of 6-HK-3-O-G scavenging hydroxyl radical, and more important reasons is the chelation of 6-HK-3-O-G with Fe2+ , which can block the Fenton reaction. Conclusions: 6-HK-3-O-G do has strong anti-oxidation activity, and the chelation of 6-HK-3-O-G with Fe2+ may play a vital role for its inhibiting Fenton chemistry under physiological conditions.

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