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作 者:袁萍[1,2] 邹学敏[1] 余明东[1] 何杰颖[1] 王友良[1] 邹云飞[3] 李东阳[1]
机构地区:[1]南华大学公共卫生学院,湖南衡阳421001 [2]长沙医学院 [3]皖南医学院
出 处:《南华大学学报(医学版)》2010年第6期746-749,共4页Journal of Nanhua University(Medical Edition)
基 金:湖南省教育厅科研基金资助项目(编号:09C142)
摘 要:目的探讨茶多酚对甲醛致人内皮细胞氧化损伤的保护作用。方法采用体外常规培养内皮细胞,取对数生长期的细胞进行实验。实验设对照组、甲醛损伤组和低、中、高剂量茶多酚保护组,其中茶多酚先与细胞预孵12 h后加入0.1 mmol/L甲醛,置CO_2培养箱培养4 h,检测细胞培养液中SOD活力及LDH、MDA、NO的含量,SP法检测NF-κB。结果茶多酚各保护组与甲醛损伤组比较SOD活力明显升高,LDH、MDA含量均降低(P<0.05);茶多酚各保护组内皮细胞NO释放量减少、NF-κB表达明显下降与甲醛损伤组比较均有显著性(P<0.05)。结论茶多酚可提高内皮细胞抗氧化酶的活性,减轻甲醛所致的氧化损伤;茶多酚通过拆制NF-κB的表达,减少NO的产生从而减轻细胞内脂质过氧化是其保护作用的重要机制。Objective To investigate the protective effect of tea polyphenols on oxidative damaged endothelial cells induced by Formaldehyde.Methods Human umbilical vein endothelial cells(HUVEC - 12) were cultured with DMEM in vitro and the cells in the exponential phase of growth to experiment were selected.They were divided into nomal cells group, formaldehyde -induced injury group(0.1 mmol/L),low,medium and high doses of Tea Polyphenols protection group.The cells were pre -incubated with tea polyphenols,after 12 h,adding 0.1 mmol/L formaldehyde and put in CO_2 Incubators foster home for 4h,then the SOD activity and LDH,MDA and NO contention of the cell culture medium were detected, method of SP was used to detect NF -κB.Results SOD activity of the tea Polyphenols protection groups were higher than the formaldehyde injury group actively;LDH,MDA levels were lower than formaldehyde - induced injury group,the differences were statistically significant(P0.05);The NO levels of tea Polyphenols protection groups were lower,NF -κB's activity declined actively compared with the formaldehyde - induced injury group significantly,the differences were statistically significant(P0.05).Conclusion Tea polyphenols can increase the activity of antioxidant enzymes of endothelial cells and reduce oxidative damage caused by fomaldehyde;The important mechanism of tea polyphenols' protective effection is to inhibit the expression of NF -κB and reduce NO generation which lightens the intracellular lipid peroxidation.
关 键 词:人脐静脉内皮细胞(HUVEC-12) 茶多酚 甲醛 氧化损伤
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