食品科学 ›› 2018, Vol. 39 ›› Issue (1): 238-242.doi: 10.7506/spkx1002-6630-201801036

• 营养卫生 • 上一篇    下一篇

水飞蓟素对丙烯酰胺诱导人肝癌细胞氧化损伤的保护作用

李 亮1,赵筱铎1,刘 巍2,孙红洋1,赵洪宇1,邵美丽1,*   

  1. 1.东北农业大学食品学院,黑龙江 哈尔滨 150030;2.同江出入境检验检疫局,黑龙江 同江 156400
  • 出版日期:2018-01-15 发布日期:2018-01-05
  • 基金资助:
    黑龙江省自然科学基金面上项目(C201303);黑龙江省教育厅自然科学基金项目(12541045)

Protective Effect of Silymarin on Acrylamide-Induced Oxidative Damage in HepG2 Cells

LI Liang1, ZHAO Xiaoduo1, LIU Wei2, SUN Hongyang1, ZHAO Hongyu1, SHAO Meili1,*   

  1. 1. College of Food Science, Northeast Agricultural University, Harbin 150030, China; 2. Tongjiang Entry-Exit Inspection and Quarantine Bureau, Tongjiang 156400, China
  • Online:2018-01-15 Published:2018-01-05

摘要: 研究水飞蓟素对人肝癌细胞系(human hepatocellular liver carcinoma cell line,HepG2)增殖的影响以及 对食品加工过程中产生的丙烯酰胺所致肝细胞毒性的预防效果,同时对其保护机制进行探讨。通过噻唑蓝法检测 水飞蓟素对HepG2细胞增殖的影响和对丙烯酰胺诱发HepG2细胞毒性的保护效果;利用荧光探针法对HepG2细胞 内活性氧的变化进行检测,并运用比色法分别检测细胞内脂质、蛋白质及DNA的氧化损伤标志物(丙二醛、蛋 白羰基和8-羟基脱氧鸟苷)含量;利用酶活力试剂盒检测细胞内过氧化氢酶(catalase,CAT)、超氧化物歧化酶 (superoxide dismutase,SOD)和谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)活力的变化。结果显示, 12~96 μg/mL的水飞蓟素对HepG2细胞无毒性;水飞蓟素可以抑制丙烯酰胺引起的细胞存活率降低和氧自由基水平 升高,减少丙烯酰胺对脂质、蛋白质和DNA的氧化损伤,并提高细胞内抗氧化物酶CAT、SOD和GSH-Px活力。研 究证明,水飞蓟素能够缓解丙烯酰胺对肝细胞造成的氧化损伤。

关键词: 水飞蓟素, 丙烯酰胺, 人肝癌细胞系

Abstract: This study was designed to study the effect of silymarin on the proliferation of human hepatocellular liver carcinoma cell line (HepG2) and its preventive effect on the hepatotoxicity caused by acrylamide produced during food processing and to discuss the underlying mechanism. The effect of silymarin on the proliferation of HepG2 cells and its protective effect on acrylamide-induced cytotoxicity in HepG2 cells were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay. By use of fluorescence probe 2,7-dichlorodi-hydrofluorescein diacetate (DCFHDA) method, the change in intracellular reactive oxygen species (ROS) of HepG2 cells was detected, and the markers of oxidative damage to lipid, protein and DNA (malondialdehyde, protein carbonyl and 8-hydroxy-2’-deoxyguanosine) were colorimetrically detected. The activities of the intracellular antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured with commercial kits. Our data revealed that the silymarin at 12–96 μg/mL had no cytotoxic effect on HepG2 cells and could increase cell viability and the enzyme activities of CAT, SOD and GSH-Px, reducing intracellular ROS levels and oxidative damage induced by acrylamide to lipid, protein and DNA in HepG2 cells. Therefore, silymarin can protect hepatic cells from oxidative damage caused by food-derived acrylamide.

Key words: silymarin, acrylamide, HepG2

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