Ginsenoside Rg1 promotes bone marrow stromal cells proliferation via the activation of the estrogen receptor-mediated signaling pathway
Aim: To investigate the possible mechanisms of ginsenoside Rg1 promoting bone marrow stromal cell (BMSC) proliferation. Methods: BMSC were isolated from bone marrow of Sprague-Dawley rats and maintained in vitro. After stimulation with 1 mol/L ginsenoside Rg1 for the indicated time, the proliferation ability of BMSC were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and [3 H]-thymidine incorporation assays. The estrogen receptor (ER) binding activity of BMSC was determined by a specific ER antagonist and an ER binding assay. Furthermore, the influence of ginsenoside Rg1 on the expression of ERα was investigated by RT-PCR and Western blotting assays. Results: BMSC proliferation stimulated by 1 mol/L ginsenoside Rg1 can be completely blocked by 1 mol/L ER antagonist ICI 182, 780, or ERα-specific antagonist methylpiperidinopyrazole. Moreover, Rg1 failed to displace the specific binding of [3 H]17 -estradiol to BMSC cell lysates, suggesting that no direct interaction of Rg1 with the ER is needed for its estrogenic effects. In addition, 1 mol/L Rg1 had no effects on the expression of ERα in either the mRNA or protein levels. Conclusion: Our results indicate that ERα is essential for mediating the effects of Rg1 on stimulating BMSC proliferation, which might involve the ligand/receptor-independent activation of ERα.
Document Type: Research Article
Affiliations: 1: Department of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China 2: Department of Clinical Laboratory Medicine, Nanjing Benq Hospital, Nanjing 210029, China 3: Department of Medicine, Baylor College of Medicine, Houston, Texas, USA 4: Department of Internal Medicine, the Hospital Affiliated with Shanghai Meishan Group, Nanjing 210039, China 5: Department of Pharmacology, Nanjing Medical University, Nanjing 210029, China
Publication date: 2008-10-01