食品科学 ›› 2020, Vol. 41 ›› Issue (5): 159-165.doi: 10.7506/spkx1002-6630-20190101-013

• 营养卫生 • 上一篇    下一篇

小米糠黄酮对H2O2致HepG2氧化应激损伤的保护作用

郭增旺,樊乃境,田海芝,滕飞,李萌,李杨,王中江,江连洲   

  1. (1.东北农业大学食品学院,黑龙江 哈尔滨 150030;2.山东禹王生态食业有限公司,山东 禹城 253000)
  • 出版日期:2020-03-15 发布日期:2020-03-23
  • 基金资助:
    黑龙江省自然科学基金面上项目(C2018024);山东省泰山产业领军人才工程高效生态农业创新类项目(LJNY201607); “大禹英才”项目;黑龙江省应用技术研究与开发技术重大项目(GA17B002)

Protective Effects of Flavonoids from Millet Bran on H2O2-Induced Oxidative Stress Injury in HepG2 Cells

GUO Zengwang, FAN Naijing, TIAN Haizhi, TENG Fei, LI Meng, LI Yang, WANG Zhongjiang, JIANG Lianzhou   

  1. (1. School of Food Science, Northeast Agricultural University, Harbin 150030, China; 2. Shandong Yuwang Ecological Food Co. Ltd., Yucheng 253000, China)
  • Online:2020-03-15 Published:2020-03-23

摘要: 目的:研究小米糠黄酮对H2O2致HepG2细胞氧化损伤的修复作用及其机制。方法:实验分为正常组、氧化应激模型组以及小米糠黄酮低、中、高剂量组,测定小米糠黄酮对H2O2诱导构建氧化应激损伤模型的细胞增殖率、胞内活性氧水平、抗氧化物酶系和凋亡蛋白表达量的影响。结果表明:小米糠黄酮显著缓解H2O2对HepG2造成的细胞生长抑制(P<0.05),显著降低胞内活性氧和丙二醛的水平(P<0.05),显著提高超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶活力(P<0.05),并且显著下调bax、p53、Caspase-3凋亡蛋白的表达量(P<0.05)。小米糠黄酮对H2O2致HepG2氧化应激损伤具有保护作用,其作用机制可能和抑制细胞凋亡通路蛋白的表达,调控细胞的氧化还原系统、清除胞内活性氧水平、提高胞内抗氧化酶系的活性有关。

关键词: 小米糠黄酮, 氧化应激, 抗氧化物酶系, 凋亡通路

Abstract: In this paper, we aimed to study the protective effect and mechanism of flavonoids from millet bran (FMB) on H2O2-induced oxidative damage in HepG2 cells by determining cell proliferation rate, intracellular reactive oxygen species (ROS) level, antioxidant enzymes activities and the expression of apoptosis-related proteins. The experiment was divided into normal group, oxidative stress model group, and low-, medium- and high-dose FMB treatment groups. The results showed that FMB significantly alleviated cell growth inhibition induced by H2O2 in HepG2 cells, decreased the levels of intracellular ROS and malondialdehyde (MDA), and increased the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), as well as down-regulated the expression of bax, p53, and caspase-3 (P < 0.05). Consequently, FMB could protect HepG2 cells against H2O2-induced oxidative damage, and its underlying mechanism may be related to inhibiting the expression of apoptosis-related proteins, regulating the cellular redox system, scavenging intracellular ROS, and increasing the activities of intracellular antioxidant enzymes.

Key words: flavonoids from millet bran, oxidative stress, antioxidant enzyme system, apoptotic pathways

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