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Ginsenoside-Rb1 Acts as a Weak Phytoestrogen in MCF-7 Human Breast Cancer Cells
YoungJooLee,YoungRanJin,임원청,WanKyuPark,JungYoonCho,SiyoulJang,이승기 대한약학회 2003 Archives of Pharmacal Research Vol.26 No.1
Ginseng has been recommended to alleviate the menopausal symptoms, which indicates that components of ginseng very likely contain estrogenic activity. We have examined the possibility that a component of Panax ginseng, ginsenoside-Rb1, acts by binding to estrogen receptor. We have investigated the estrogenic activity of ginsenoside-Rb1 in a transient transfection system using estrogen-responsive luciferase plasmids in MCF-7 cells. Ginsenoside- Rb1 activated the transcription of the estrogen-responsive luciferase reporter gene in MCF-7 breast cancer cells at a concentration of 50 mM. Activation was inhibited by the specific estrogen receptor antagonist ICI 182,780, indicating that the estrogenic effect of ginsenoside-Rb1 is estrogen receptor dependent. Next, we evaluated the ability of ginsenoside-Rb1 to induce the estrogen-responsive gene c-fos by semi-quantitative RT-PCR assays and Western analyses. Ginsenoside-Rb1 increased c-fos both at mRNA and protein levels. However, ginsenoside- Rb1 failed to activate the glucocorticoid receptor, the retinoic acid receptor, or the androgen receptor in CV-1 cells transiently transfected with the corresponding steroid hormone receptors and hormone responsive reporter plasmids. These data support our hypothesis that ginsenoside- Rb1 acts a weak phytoestrogen, presumably by binding and activating the estrogen receptor.
Ginsenoside Rc and Re Stimulate c-Fos Expression in MCF-7 Human Breast Carcinoma Cells
YoungJooLee,YoungRanJin,임원청,SangMiJi,JungYoonCho,반재준,이승기 대한약학회 2003 Archives of Pharmacal Research Vol.26 No.1
We have found that ginsenoside Rc and Re induce c-fos in MCF-7 human breast carcinoma cells at both the mRNA and protein levels. However, neither ginsenoside activated the expression of reporter gene under the control of AP-1/TPA response elements. We have also examined the possibility that ginsenoside Rc and Re act by binding to intracellular steroid hormone receptors that act as transcriptional factors in the nucleus in inducing c-fos mRNA in MCF7 human breast carcinoma cells. However, ginsenoside Rc and Re did not bind to glucocorticoid, androgen, estrogen, or retinoic acid receptors as examined by the transcription activation of the luciferase reporter genes in CV-1 cells that were transiently transfected with the corresponding steroid hormone receptors and hormone responsive luciferase reporter plasmids. These data demonstrate that ginsenoside Rc and Re act via other transcription factors and not via estrogen receptor in c-Fos expression.