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Retracted : Radix Paeoniae Alba increases serum estrogen level and up‐regulates estrogen receptor expression in uterus and vagina of immature/ovariectomized mice
Author(s) -
Xu Ying,
Li Xin,
Chen Ting,
Qu Yakun,
Zheng Hongxia,
Zhang Zijia,
Zhao Yuan,
Lin Na
Publication year - 2019
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.6205
Subject(s) - ovariectomized rat , estrogen , endocrinology , medicine , estrogen receptor , uterus , estrogen receptor beta , estrogen receptor alpha , luteinizing hormone , vaginal atrophy , biology , chemistry , hormone , cancer , breast cancer
Radix Paeoniae Alba (RPA) is widely used in clinical treatment for gynecological diseases, particularly abnormal menstruation, menstrual pain, and breast tenderness; however, no scientific evidence base links RPA to estrogen replacement therapy. In this study, we characterize estrogenic activity of RPA using immature and ovariectomized (OVX) mice together with in vitro studies focus on estrogen receptor (ER) pathway for molecular mechanism. RPA treatments demonstrated significant estrogenic activity, as indicated by promoting the development of uterus and vagina in immature mice, reversing the atrophy of uterus and vagina in OVX mice, up‐regulating the expressions of ERα and ERβ at protein and mRNA level in reproductive tissues. Meanwhile, RPA significantly increased serum estradiol and clearly decreased serum luteinizing hormone and follicle‐stimulating hormone of immature/OVX mice. Moreover, RPA could induce ER positive MCF‐7 cell from S‐phase to G2 stage and induce proliferation and no influence on ER negative MDA‐MB‐231 cell. RPA could bind with ERα and ERβ and significantly stimulate ERα/β‐estrogen response element (ERE) luciferase reporter gene expression. All activities were inhibited by the ER antagonist ICI 182,780. This study illustrates RPA exerts estrogenic effects by stimulating biosynthesis of estrogen in circulation, up‐regulating ERs in target tissues, and mimicking the estrogen through ER‐ERE‐dependent pathway.