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Vitisin B stimulates osteoblastogenesis via estrogen receptor

 

Yu-Ling Huang 1,2, Wen-Fei Chiou 1, 3,4,*

  

1 National Research Institute of Chinese Medicine, Taipei, Taiwan

2 Department of Cosmetic Science, Chang Gung University of Science and Technology, Taoyuan, Taiwan

3 Department of Biotechnology, Hungkuang University, Taichung, Taiwan

4 Ph.D Program for the Clinical Drug Discovery from Botanical Herbs, Taipei Medical University, Taipei, Taiwan 

Vitisin B is one of the major components existed in Vitis thunbergii, a herbal medicine used in Taiwan for treatment of inflammatory bone diseases. The present study further delineated the action mechanism(s) by which vitisin B stimulates osteoblastogenesis by using MC3T3-E1 cells. Results showed that vitisin B evoked estrogen receptor (ER)-dependent increases in alkaline phosphatase (ALP) activity, bone mineralization, mRNA expression of osteoblast-characteristic genes (collagen type I, bone morphogenetic protein 2, bone sialprotein and osteocalcin) and transcription factors (Runx2 and osterix) in MC3T3-E1 cells. Vitisin B and 17b-estradiol (E2) both induced ER-mediated rapid phosphorylation of Src kinase. Furthermore, the rapid estrogenic phosphorylation, the expression of osteoblast-characteristic genes and final bone mineralization were all blocked in the presence of PP2. After investigation the involvement of MAPKs results demonstrated that vitisin B also evoked a Src-mediated phosphorylation of p38 and ERK through ER-dependent pathway. These findings indicated that vitisin B exerts anabolic effects in bone possibly by activating non-genomic signaling pathway through ER-mediated activation of Src kinase. Its ability to prevent ovariectomy-induced bone loss supports its use as an alternative regimen for management of postmenopausal osteoporosis.

 

Key words: Vitisin B, Osteoblast, Osteoids, Runx2, Osterix, Estrogen receptor, Src