DOI QR코드

DOI QR Code

Nectandrin A Enhances the BMP-Induced Osteoblastic Differentiation and Mineralization by Activation of p38 MAPK-Smad Signaling Pathway

  • Kim, Do Yeon (Department of Pharmacology and Clinical Pharmacy, College of Pharmacy, Kyung Hee University) ;
  • Kim, Go Woon (Department of Pharmacology and Clinical Pharmacy, College of Pharmacy, Kyung Hee University) ;
  • Chung, Sung Hyun (Department of Pharmacology and Clinical Pharmacy, College of Pharmacy, Kyung Hee University)
  • 투고 : 2013.07.14
  • 심사 : 2013.09.23
  • 발행 : 2013.10.30

초록

Osteoblastic activity of nectandrin A was examined in C2C12 cells. Nectandrin A enhances the BMP-induced osteoblastic differentiation and mineralization, manifested by the up-regulation of differentiation markers (alkaline phosphatase and osteogenic genes) and increased calcium contents. In C2C12 cells co-transfected with expression vector encoding Smad4 and Id1-Luc reporter, nectandrin A increased Id1 luciferase activity in a concentration-dependent manner, when compared to that in BMP-2 treated cells, indicating that Smad signaling pathway is associated with nectandrin A-enhanced osteoblastic differentiation in C2C12 cells. In addition, nectandrin A activated p38 mitogen-activated protein kinase (MAPK) in time- and concentration-dependent manners, and phosphorylated form of pSmad1/5/8 and alkaline phosphatase activity were both decreased when the cells were pretreated with SB203580, a p38 MAPK inhibitor, suggesting that p38 MAPK might be an upstream kinase for Smad signaling pathway. Taken together, nectandrin A enhances the BMP-induced osteoblastic differentiation and mineralization of C2C12 cells via activation of p38 MAPK-Smad signaling pathway, and it has a therapeutic potential for osteoporosis by promoting bone formation.

키워드

참고문헌

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