摘要
以橙皮苷为原料,经三氯化铝-吡啶去甲基反应合成药用天然产物圣草次苷,产物通过1H核磁共振(nuclear magnetic resonance,NMR)和13C NMR进行结构确证,并探究其对过氧化氢(H_(2)O_(2))诱导氧化应激损伤的人脐静脉内皮细胞系(human umbilical vein endothelial cells,HUVEC)细胞的保护作用机制。结果表明:圣草次苷对HUVEC细胞无毒性作用,能显著提高氧化损伤HUVEC细胞的存活率(P<0.05),但无显著剂量效应;显著降低细胞中活性氧水平和丙二醛含量(P<0.05),显著提高超氧化物歧化酶、谷胱甘肽过氧化物酶、过氧化氢酶等抗氧化酶的活力(P<0.05);显著上调Bcl-2/Bax蛋白比值和下调p53蛋白表达(P<0.05)。结论:圣草次苷能有效阻止H_(2)O_(2)所致HUVEC细胞损伤,该作用与圣草次苷的抗氧化活性和抑制细胞死亡有关。
Eriocitrin was successfully synthesized by aluminum trichloride-pyridine demethylation reaction from hesperidin,as confirmed by 1H and 13C nuclear magnetic resonance(NMR),to explore its protective effect and mechanism on human umbilical vein endothelial cells(HUVEC)from hydrogen peroxide(H_(2)O_(2))-induced oxidative damage.The results showed that eriocitrin had no toxic effect on cells HUVEC,and even significantly promoted the survival of HUVEC cells suffering from oxidative stress though without clear dose dependence(P<0.05).Eriocitrin significantly reduced the levels of reactive oxygen species(ROS)and malondialdehyde(MDA)content(P<0.05),increased antioxidant enzyme activities(superoxide dismutase,glutathion peroxidase and catalase)(P<0.05),up-regulated Bcl-2/Bax protein ratio(P<0.05)and downregulated p53 protein expression(P<0.05).It is suggested that eriocitrin can effectively prevent H_(2)O_(2)-caused damage to HUVEC cells,which is related to its antioxidant activity and inhibition on cell death.
作者
梁曾恩妮
汪秋安
张菊华
苏东林
付复华
李高阳
刘伟
单杨
LIANG Zeng’enni;WANG Qiuan;ZHANG Juhua;SU Donglin;FU Fuhua;LI Gaoyang;LIU Wei;SHAN Yang(Institute of Agricultural Product Processing,Hunan Academy of Agricultural Sciences,Changsha 410125,China;Hunan Key Laboratory of Fruits&Vegetables Storage,Processing and Quality Safety,Changsha 410125,China;College of Chemistry and Chemical Engineering,Hunan University,Changsha 410082,China)
出处
《食品科学》
EI
CAS
CSCD
北大核心
2021年第15期159-166,共8页
Food Science
基金
湖南省农业科技创新资金项目(2019JG01
2020CX47)
“十二五”国家科技支撑计划项目(2012BAD31B02)
湖南省重点研发计划项目(2019NK2041)。
关键词
圣草次苷
合成
氧化损伤
人脐静脉内皮细胞
eriocitrin
synthesis
oxidative damage
human umbilical vein endothelial cells