A ginsenoside-Rh1, a component of ginseng saponin, activates estrogen receptor in human breast carcinoma MCF-7 cells

Lee, Young‐Joo; Jin, YoungRan; Lim, Wonchung; Ji, SangMi; Choi, Seungjin; Jang, Siyoul; Lee, SeungKi

doi:10.1016/s0960-0760(03)00067-0

Cited by 143 publications

(75 citation statements)

References 23 publications

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“…In the work of Bae et al [63], the proliferation of MCF-7 cells increased 2.1-fold at the concentration of 1 µM of G-Rh1 to reach the same level as 1 nM of 17β-estradiol. The expressions of c-fos and pS2 genes were also slightly induced in the presence of G-Rh1, as previously reported [62]. Taken together, these data consistently demonstrated G-Rh1 as a weak estrogenic compound.…”

Section: Estrogenic Activitysupporting

confidence: 89%

“…Dong et al [61] observed that G-Rh1 stimulated cell proliferation in a dose-dependent manner, reaching a significant level at 100 µM with a significant correlation (r = 0.218, p < 0.05) between G-Rh1 and 17β-estradiol in the expression profiles after treatment of MCF-7 cells with these two compounds. Lee et al [62] demonstrated that G-Rh1 bound to and activated the estrogen receptor at an extent of 5000-to 10 000-fold weaker than that of 17β-estradiol. In the work of Bae et al [63], the proliferation of MCF-7 cells increased 2.1-fold at the concentration of 1 µM of G-Rh1 to reach the same level as 1 nM of 17β-estradiol.…”

Section: Estrogenic Activitymentioning

confidence: 99%

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Ginsenoside Rh1: A Systematic Review of Its Pharmacological Properties

et al. 2018

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Supporting information available online at http://www.thieme-connect.de/products ABSTR AC TGinsenoside Rh1 is one of major bioactive compounds extracted from red ginseng, which has been increasingly used for enhancing cognition and physical health worldwide. The objective of this study was to review the pharmacological effects of ginsenoside Rh1 in a systematic manner. We performed searches on eight electronic databases including MEDLINE (Pubmed), Scopus, Google Scholar, POPLINE, Global Health Library, Virtual Health Library, the System for Information on Grey Literature in Europe, and the New York Academy of Medicine Grey Literature Report to select the original research publications reporting the biological and pharmacological effects of ginsenoside Rh1 from in vitro and in vivo studies regardless of publication language and study design. Upon applying the inclusion and exclusion criteria, we included a total of 57 studies for our systemic review. Ginsenoside Rh1 exhibited the potent characteristics of anti-inflammatory, antioxidant, immunomodulatory effects, and positive effects on the nervous system. The cytotoxic effects of ginsenoside Rh1 were dependent on different types of cell lines. Other pharmacological effects including estrogenic, enzymatic, anti-microorganism activities, and cardiovascular effects have been mentioned, but the results were considerably diverged. A higher quality of evidence on clinical trial studies is highly recommended to confirm the consistent efficacy of ginsenoside Rh1.

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Section: Estrogenic Activitysupporting

confidence: 89%

Section: Estrogenic Activitymentioning

confidence: 99%

Ginsenoside Rh1: A Systematic Review of Its Pharmacological Properties

et al. 2018

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“…12 The only study to address the question of extraction method and ginseng's estrogenic effects found that both a methanol and water extract of P quinquefolium bound ERα and ERβ isoforms with different affinities depending on the source of the root and that this activity may be attributed to the presence of the mycotoxin zearalenone in root extracts; however, the extract with the lowest zearalenone concentration exhibited the highest ER binding affinity of the 2 P quinquefolium samples tested. 15 Other studies have examined the estrogenicity of specific ginsenosides and determined that ginsenoside Rh1 induced estrogenic effects in MCF-7 cells due to direct ER interaction, 22 whereas the estrogenlike effect of ginsenoside Rg1 in ER-positive breast cancer cells was not dependent on ER binding. 21,31 In fact, ginsenoside Rg1 was recently shown to stimulate MCF-7 cell proliferation and pS2 mRNA expression through activation of cross-talk between ER-and insulin growth factor 1 receptor-dependent pathways.…”

Section: Discussionmentioning

confidence: 99%

“…The ability of higher concentrations of alc-GE to inhibit cell proliferation cannot be explained by ER modulation, as ginseng/ginsenosides inhibit the proliferation of a number of cancer cell lines, most of which do not express estrogen receptors. [32][33][34][35] The estrogenic effects of low concentrations of alc-GE may be mediated by those ginsenosides known to elicit estrogenic responses, such as Rb1, Rh1, or Rg1, [21][22][23][24]36 or other unknown steroidal compounds that are of necessary abundance to elicit a response. The estrogenic ginsenoside Rb1 is one of the most abundant ginsenosides found in methanol-extracted P quinquefolium root.…”

Section: Discussionmentioning

confidence: 99%

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Extraction-Dependent Effects of American Ginseng (Panax quinquefolium) on Human Breast Cancer Cell Proliferation and Estrogen Receptor Activation

2006

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Hypothesis:Ginseng root extracts and the biologically active ginsenosides have been shown to inhibit proliferation of human cancer cell lines, including breast cancer. However, there are conflicting data that suggest that ginseng extracts (GEs) may or may not have estrogenic action, which might be contraindicated in individuals with estrogen-dependent cancers. The current study was designed to address the hypothesis that the extraction method of American ginseng (Panax quinquefolium) root will dictate its ability to produce an estrogenic response using the estrogen receptor (ER)-positive MCF-7 human breast cancer cell model. Methods: MCF-7 cells were treated with a wide concentration range of either methanol-(alc-GE) or water-extracted (w-GE) ginseng root for 6 days. Cells were grown in media containing either normal or charcoal-stripped fetal calf serum to limit exposure to exogenous estrogen. Thus, an increase in MCF-7 cell proliferation by GE indicated potential estrogenicity. This was confirmed by blocking GE-induced MCF-7 cell proliferation with ER antagonists ICI 182,780 (1 nM) and 4-hydroxytamoxifen (0.1 µ µM). Furthermore, the ability of GE to bind ERα α or ERβ β and stimulate estrogen-responsive genes was examined. Results: Alc-GE, but not w-GE, was able to increase MCF-7 cell proliferation at low concentrations (5-100 µ µg/mL) when cells were maintained under low-estrogen conditions. The stimulatory effect of alc-GE on MCF-7 cell proliferation was blocked by the ER antagonists ICI 182,780 or 4-hydroxytamoxifen. At higher concentrations of GE, both extracts inhibited MCF-7 and ER-negative MDA-MB-231 cell proliferation regardless of media conditions. Binding assays demonstrated that alc-GE, but not w-GE, was able to bind ERα α and ERβ β. Alc-GE (50 µ µg/mL) also induced an approximate 2.5-fold increase in expression of the estrogenresponsive pS2 gene, as well as progesterone receptor (PgR) gene expression, whereas w-GE was without effect. Conclusion: These data indicate that low concentrations of alc-GE, but not w-GE, elicit estrogenic effects, as evidenced by increased MCF-7 cell proliferation, in a manner antagonized by ER antagonists, interactions of alc-GE with estrogen receptors, and increased expression of estrogenresponsive genes by alc-GE. Thus, discrepant results between different laboratories may be due to the type of GE being analyzed for estrogenic activity.

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Nutritional Management of Oncologic Diseases

Mauldin

2023

Applied Veterinary Clinical Nutrition

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A ginsenoside-Rh1, a component of ginseng saponin, activates estrogen receptor in human breast carcinoma MCF-7 cells

Cited by 143 publications

References 23 publications

Ginsenoside Rh1: A Systematic Review of Its Pharmacological Properties

Ginsenoside Rh1: A Systematic Review of Its Pharmacological Properties

Extraction-Dependent Effects of American Ginseng (Panax quinquefolium) on Human Breast Cancer Cell Proliferation and Estrogen Receptor Activation

Nutritional Management of Oncologic Diseases

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