Ginsenoside Rgl promotes bone marrow stromal cells proliferation via the activation of the estrogen receptor-mediated signaling pathway  

作　　者：Xin-zheng LU Jun-hong WANG Xin WU Lei ZHOU Li WANG Xiao-wen ZHANG Ke-jiang CAO Jun HUANG 

机构地区：[1]Department of Cardiology the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China [2]Department of Medicine, Baylor College of Medicine, Houston, Texas, USA [3]Department of Clinical Laboratory Medicine, Nanjing Benq Hospital, Nanjing 210029, China [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

出　　处：《Acta Pharmacologica Sinica》2008年第10期1209-1214,共6页中国药理学报（英文版）

基　　金：This work was supported by the National Natural Science Foundation of China （No 30370575）, a post-doctoral grant of Jiangsu Province （No 2004B21）, and the Post-Graduate Innovation Projects of Jiangsu Province （No JX22013013）. Author contribution Xin-zheng LU designed research; Jun-hong WANG, Xin WU, and Li WANG performed research; Li WANG, contrbuted new analytical tools and reagents; Xiao-Wen ZHANG analyzed data; Jun-hong WANG and Lei ZHOU wrote the paper.

摘　　要：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 μmol/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 μmol/L ginsenoside Rg1 can be completely blocked by 1 μmol/L ER antagonist ICI 182, 780, or ERα- specific antagonist methylpiperidinopyrazole. Moreover, Rg1 failed to displace the specific binding of [3^H] 17β-estradiol to BMSC cell lysates, suggesting that no direct interaction of Rg1 with the ER is needed for its estrogenic effects. In addition, 1μmol/L Rg1 had no effects on the expression of ERα in either the mRNA or protein levels. Conelusion： 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.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 μmol/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 μmol/L ginsenoside Rg1 can be completely blocked by 1 μmol/L ER antagonist ICI 182, 780, or ERα- specific antagonist methylpiperidinopyrazole. Moreover, Rg1 failed to displace the specific binding of [3^H] 17β-estradiol to BMSC cell lysates, suggesting that no direct interaction of Rg1 with the ER is needed for its estrogenic effects. In addition, 1μmol/L Rg1 had no effects on the expression of ERα in either the mRNA or protein levels. Conelusion： 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.

关 键 词：ginsenoside Rgl bone marrow stromal cell estrogen receptor PROLIFERATION 

分 类 号：R977[医药卫生—药品]