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Ginsenoside Rh2(S) induces the differentiation and mineralization of osteoblastic MC3T3-E1 cells through activation of PKD and p38 MAPK pathways

  • Kim, Do-Yeon (Department of Pharmacology and Clinical Pharmacy, College of Pharmacy, Graduate School of Kyung Hee University) ;
  • Jung, Mi-Song (Department of Pharmacology and Clinical Pharmacy, College of Pharmacy, Graduate School of Kyung Hee University) ;
  • Park, Young-Guk (Department of Orthodontics, School of Dentistry, Graduate School of Kyung Hee University) ;
  • Yuan, Hai Dan (Department of Pharmacology and Clinical Pharmacy, College of Pharmacy, Graduate School of Kyung Hee University) ;
  • Quan, Hai Yan (Department of Pharmacology and Clinical Pharmacy, College of Pharmacy, Graduate School of Kyung Hee University) ;
  • Chung, Sung-Hyun (Department of Pharmacology and Clinical Pharmacy, College of Pharmacy, Graduate School of Kyung Hee University)
  • Received : 2011.07.06
  • Accepted : 2011.07.29
  • Published : 2011.10.31

Abstract

As part of the search for biologically active anti-osteoporotic agents that enhance differentiation and mineralization of osteoblastic MC3T3-E1 cells, we identified the ginsenoside Rh2(S), which is an active component in ginseng. Rh2(S) stimulates osteoblastic differentiation and mineralization, as manifested by the up-regulation of differentiation markers (alkaline phosphatase and osteogenic genes) and Alizarin Red staining, respectively. Rh2(S) activates p38 mitogen-activated protein kinase (MAPK) in time- and concentration-dependent manners, and Rh2(S)-induced differentiation and mineralization of osteoblastic cells were totally inhibited in the presence of the p38 MAPK inhibitor, SB203580. In addition, pretreatment with Go6976, a protein kinase D (PKD) inhibitor, significantly reversed the Rh2(S)-induced p38 MAPK activation, indicating that PKD might be an upstream kinase for p38 MAPK in MC3T3-E1 cells. Taken together, these results suggest that Rh2(S) induces the differentiation and mineralization of MC3T3-E1 cells through activation of PKD/p38 MAPK signaling pathways, and these findings provide a molecular basis for the osteogenic effect of Rh2(S).

Keywords

References

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