Food and Nutrition Sciences

Volume 5, Issue 2 (January 2014)

ISSN Print: 2157-944X   ISSN Online: 2157-9458

Google-based Impact Factor: 0.92  Citations  h5-index & Ranking

(–)-Epigallocatechingallate Interferes RANKL/RANK Signal Pathway and Induces Apoptosis during Osteoclastogenesis in RAW264 Cell

HTML  XML Download Download as PDF (Size: 833KB)  PP. 107-116  
DOI: 10.4236/fns.2014.52014    3,947 Downloads   5,340 Views  Citations

ABSTRACT

Green tea catechin, (–)-epigallocatechin-3-gallate [(–)-EGCG], was found to increase osteogenic functioning in mesenchymal stem cells. This study qualified EGCG, the strongest inhibitory efficiency for receptor activator of nuclear factor-κB (NF-κB) ligand (RANKL)-activated osteoclastogenesis among other green tea catechins for RAW264, a murine preosteoclast cell line. Moreover, EGCG inhibited tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cell formation dose dependently in both single culture and co-culture systems, the expression of transcription factor, nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1) and some osteoclastic genes. Especially, EGCG exhibited a strong inhibitory effect on the expression levels of RANK, the receptor of RANKL, and OSCAR, a key co-stimulator of the RANKL/RANK signal. Simultaneously, apoptotic genes expression and Hoechst staining revealed that EGCG induced apoptosis in RAW264. Taken together, these data suggest that the inhibitory effect of EGCG to osteoclastogenesis is associated with a down regulation of RANKL/RANK signal, and increased apoptosis of preosteoclasts.

Share and Cite:

R. Zhao, M. Kamon and K. Sakamoto, "(–)-Epigallocatechingallate Interferes RANKL/RANK Signal Pathway and Induces Apoptosis during Osteoclastogenesis in RAW264 Cell," Food and Nutrition Sciences, Vol. 5 No. 2, 2014, pp. 107-116. doi: 10.4236/fns.2014.52014.

Copyright © 2024 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.