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Phytoestrogen alpha-zearalanol inhibits homocysteine-induced endothelin-1 expression and oxidative stress in human umbilical vein endothelial cells.

Phytoestrogen alpha-zearalanol inhibits homocysteine-induced endothelin-1 expression and oxidative stress in human umbilical vein endothelial cells. Research Abstract Details 

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  • Phytoestrogen alpha-zearalanol inhibits homocysteine-induced endothelin-1 expression and oxidative stress in human umbilical vein endothelial cells. Abstract Text:

    jinhong duanJinhong Duan,haishan xuHaishan Xu,shunling daiShunling Dai,xiaoming wangXiaoming Wang,yunqing wuYunqing Wu,yandong zhangYandong Zhang,renyu sunRenyu Sun,jun renJun Ren,jinhong duanJinhong Duan,haishan xuHaishan Xu,shunling daiShunling Dai,xiaoming wangXiaoming Wang,yunqing wuYunqing Wu,yandong zhangYandong Zhang,renyu sunRenyu Sun,jun renJun Ren,

    Although estrogen replacement therapy may improve dampened endothelial function in postmenopausal women, the associated risk of breast and ovarian cancer has limited its long-term use. Identifying effective alternative remedy with less carcinogenicity is in serious demand. This study was designed to examine the effect of the phytoestrogen alpha-zearalanol (alpha-ZAL) on homocysteine-induced endothelin-1 (ET-1) induction, reactive oxygen species (ROS) production and transcription pathways in human umbilical vein endothelial cells (HUVECs). ROS was measured by DCF fluorescent microscopy. Homocysteine-induced expression of ET-1 mRNA, ERK, pERK and c-jun/AP-1 protein was measured using RT-PCR and Western blot analysis, respectively. ET-1 secretion was determined by the enzymatic immunoassay. Transcriptional factor AP-1 expression in response to alpha-ZAL, homocysteine or both was evaluated by transient transfection assay. Our data revealed that alpha-ZAL ablated homocysteine-elicited ET-1 secretion, upregulated ET-1 mRNA and homocysteine-induced ROS accumulation without any effects by itself. alpha-ZAL also nullified homocysteine-induced increase in c-Jun/AP-1 expression/activity without eliciting any effect by itself. Collectively, our data indicated that alpha-ZAL may antagonize homocysteine-induced ET-1 gene induction, ROS accumulation, activation of ERK signaling pathway and AP-1 transcriptional factor, all of which may contribute to alpha-ZAL-induced beneficial effect on endothelial function.

    Phytoestrogen alpha-zearalanol inhibits homocysteine-induced endothelin-1 expression and oxidative stress in human umbilical vein endothelial cells. Publishing Authors By Initials

    j duanJ Duan,h xuH Xu,s daiS Dai,x wangX Wang,y wuY Wu,y zhangY Zhang,r sunR Sun,j renJ Ren,j duanJ Duan,h xuH Xu,s daiS Dai,x wangX Wang,y wuY Wu,y zhangY Zhang,r sunR Sun,j renJ Ren,

    For similar abstracts research abstracts see: abstracts research

    PUBMED ID PMID:

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    Phytoestrogen alpha-zearalanol inhibits homocysteine-induced endothelin-1 expression and oxidative stress in human umbilical vein endothelial cells. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: Atherosclerosis

    VOLUME: 197

    Page Numbers: 549-55

    Journal Abbreviation:

    ISSN: 1879-1484

    DAY: 27

    MONTH: 09

    YEAR: 2007

    Phytoestrogen alpha-zearalanol inhibits homocysteine-induced endothelin-1 expression and oxidative stress in human umbilical vein endothelial cells. Information

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    LANGUAGE: eng

    NlmUniqueID: 242543

    Phytoestrogen alpha-zearalanol inhibits homocysteine-induced endothelin-1 expression and oxidative stress in human umbilical vein endothelial cells. Keywords Mesh Terms:

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    Chemical & Substance for Abstract: Phytoestrogen alpha-zearalanol inhibits homocysteine-induced endothelin-1 expression and oxidative stress in human umbilical vein endothelial cells. Information

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    Grant and Affiliation Information for Phytoestrogen alpha-zearalanol inhibits homocysteine-induced endothelin-1 expression and oxidative stress in human umbilical vein endothelial cells.

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    Country: Ireland

    Ireland Research PublicationIreland Research Publication

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    MEDLINETA: Atherosclerosis

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