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Estrogenic effects of ginsenoside Rg1 in endometrial cells in vitro were not observed in immature CD-1 mice or ovariectomized mice model

Chen, Wen-Fang PhD1,2; Gao, Quan-Gui PhD1; Dai, Zhi-Jie PhD3; Kung, Annie Wai-Chee MD3; Guo, De-an PhD4; Wong, Man-Sau PhD1,5

doi: 10.1097/gme.0b013e318250361c
Original Articles

Objective The present study was designed to determine whether ginsenoside Rg1 could exert selective estrogenic effects by using both cell lines and an animal model.

Methods The endometrial Ishikawa cells and preosteoblastic MC3T3-E1 cells were treated with a different dose of Rg1. Immature CD-1 mice and ovariectomized (OVX) C57BL/6J mice were used to study the short-term and long-term estrogenic effects of Rg1, respectively.

Results Rg1 significantly increased estrogen receptor-dependent alkaline phosphatase activity, activated estrogen response element–luciferase activity, and induced the phosphorylation of mitogen-activated protein kinase kinase, extracellular-regulated kinase, and estrogen receptor-α in Ishikawa cells. In contrast, Rg1 did not induce any estrogenic responses in MC3T3-E1 cells. Administration of Rg1 to immature CD-1 mice did not alter their uterine weight or the estrogen-regulated gene expressions in the uterus. Treatment of OVX C57BL/6J mice with Rg1 via mini-osmotic pumps for 3 months did not alter the uterine weight or induce any transcriptional activation of estrogen receptor in the uterus. Rg1 induced Bcl-2 messenger RNA expression in the left ventricular tissue and striatum but failed to alter the bone mineral density in the femur and tibia of the OVX mice.

Conclusions Rg1 exerted potent estrogenic effects in endometrial cells in vitro as well as in heart and brain tissues in vivo. However, it did not exert any estrogenic effects on reproductive tissues in vivo, nor did it stimulate bone tissues in vitro or in vivo. Our results suggest that the estrogenic effects of Rg1 are distinct from those of estradiol and are cell type and tissue selective.

From the 1Department of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong SAR; 2Department of Physiology, Medical College of Qingdao University, Qingdao, PR China; 3Department of Medicine, The University of Hong Kong, Hong Kong SAR; 4National Engineering Lab of TCM Standardization, Shanghai Institute of Materia Medica, Chinese Academy of Science, Shanghai, PR China; and 5State Key Laboratory of Chinese Medicine and Molecular Pharmacology (Incubation), Shenzhen, PR China.

Received October 13, 2011; revised and accepted January 9, 2012.

Funding/support: This work was supported by the Areas of Excellence Scheme established under the University Grants Committee of the Hong Kong Special Administrative Region, China (AOE/P-10/01), the Research Grants Council General Research Fund (POLYU 5636/07M), and the Research Studentship from the Central Allocation Grant from the Research Committeeof The Hong Kong Polytechnic University.

Financial disclosure/conflicts of interest: None reported.

Address correspondence to: Man-Sau Wong, PhD, Department of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong, PRC. E-mail:

©2012The North American Menopause Society