高级检索
张小梅, 刘琳, 景立新, 仲来福. 羟基酪醇对苏丹红Ⅰ号致DNA损伤抑制作用[J]. 中国公共卫生, 2009, 25(9): 1116-1117. DOI: 10.11847/zgggws2009-25-09-51
引用本文: 张小梅, 刘琳, 景立新, 仲来福. 羟基酪醇对苏丹红Ⅰ号致DNA损伤抑制作用[J]. 中国公共卫生, 2009, 25(9): 1116-1117. DOI: 10.11847/zgggws2009-25-09-51
ZHANG Xiao-mei, LIU Lin, JING Li-xin, . Inhibitive effect of hgdroxytyrosol on Sudan Ⅰ induced DNA oxidative damage in human liver-derived HepG2 cells[J]. Chinese Journal of Public Health, 2009, 25(9): 1116-1117. DOI: 10.11847/zgggws2009-25-09-51
Citation: ZHANG Xiao-mei, LIU Lin, JING Li-xin, . Inhibitive effect of hgdroxytyrosol on Sudan Ⅰ induced DNA oxidative damage in human liver-derived HepG2 cells[J]. Chinese Journal of Public Health, 2009, 25(9): 1116-1117. DOI: 10.11847/zgggws2009-25-09-51

羟基酪醇对苏丹红Ⅰ号致DNA损伤抑制作用

Inhibitive effect of hgdroxytyrosol on Sudan Ⅰ induced DNA oxidative damage in human liver-derived HepG2 cells

  • 摘要: 目的 探讨羟基酪醇对苏丹红Ⅰ号(SudanⅠ)所致的人肝癌细胞(HepG2)DNA氧化损伤的抑制作用以及作用机制.方法 采用单细胞凝胶电泳(SCGE)检测细胞DNA氧化损伤;以21,71-二氢二氯荧光素二乙酸酯(DCFH-DA)为荧光探针检测细胞内活性氧(ROS)水平;用硫代巴比妥酸反应物(TBARS)法检测细胞内脂质过氧化水平;以免疫组化法检测细胞内8-羟基脱氧鸟苷(8-OHdG)的表达水平.结果 100μmol/L苏丹红Ⅰ号引起HepG2细胞的DNA链断裂程度尾长(46.49±2.06)μm,尾距(19.99±1.44)μm、ROS水平荧光强度(9.03±1.05)、细胞内TBARS产物(吸光度0.41±0.15)及8-OHdG表达水平(相对染色密度90.4±1.40)比对照组(二甲基亚砜)均明显增加(P<0.01);不同浓度的羟基酪醇(0,25,50,100μmol/L)分别预处理HepG2细胞30 min后,再加入100μmol/L苏丹红Ⅰ号后,羟其酪醇预处理组各项指标较单独接触苏丹红Ⅰ号组明显降低(P<0.01或P<0.05),并且呈剂量依赖关系.结论 羟基酪醇能够通过调控细胞氧化应激状态从而减轻苏丹红Ⅰ号所致的DNA氧化损伤.

     

    Abstract: Objective To explore the inhibitory effect of hydroxy tyrosol(HT)on oxidative injury induced by Sudan Ⅰin HepG2 cells.Methods The single cell gel electrophoresis assay(SCGE)was performed to study the DNA damage.The in tracellular reactive oxygen species(ROS)formation was measu redusing 2,7-dichloro fluorescein diacetate(DCFH 2DA)as a fluorescent probe.The levels of oxida tive DNA damage and lipid peroxidation were estimated by immunocy to chemistry analysis of 8-hydrocyde-oxyguanosine(8-OHdG)and by measuring the level of thtiobarbituric acid-reactive sub-stances(TBARS).Results Com pared with the control group,HepG2 cells treated with 100μMSudanⅠshowed significantly different DNA strand breaks(tail length of com et:46.49±2.06μm,the ta ilmoment:19.99±1.44μm),and the increases of ROS(9.03±1.05μm measured by fluorescent in tensity),in tracallular TBARS level(0.41±0.15μm)m easured by absorbency,and the increase of 8-OHdG expression(20.5±0.09μm measured by rleative staining intensity).Pretreatment with HT could inhibit the DNA damage and decrease the level of ROS,TBARS and 8-OHdG in a concentration-dependent manner.Conclusion HT could modulate the redox state and prevent the oxidative damage induced by SudanⅠin HepG2 cells.

     

/

返回文章
返回