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Ginsenoside Rh2 inhibits osteoclastogenesis through down-regulation of NF-κB, NFATc1 and c-Fos.
Bone. 2012 Jun; 50(6):1207-13.BONE

Abstract

Ginsenoside Rh2 is one of the most active components of red ginseng, controlling cancer and other metabolic diseases including osteoclast differentiation. However, the molecular mechanism underlying the inhibition of osteoclast differentiation by ginsenoside Rh2 remains poorly understood. In the present study, it was found that ginsenoside Rh2 suppressed osteoclast differentiation from bone marrow macrophages (BMMs) treated with receptor activator of nuclear factor κB ligand (RANKL) without any cytotoxicity. Ginsenoside Rh2 significantly reduced RANKL-induced expression of transcription factors, c-Fos and nuclear factor of activated T-cells (NFATc1), as well as osteoclast markers, TRAP and OSCAR. In defining the signaling pathways, ginsenoside Rh2 was shown to moderately inhibit NF-κB activation and ERK phosphorylation in response to RANKL stimulation in BMM cells without any effect on p38 and c-Jun N-terminal kinase (JNK). Finally, ginsenoside Rh2 blocked osteoporosis in vivo as confirmed by restored bone mineral density (BMD) and other markers associated osteoclast differentiation. Hence, it is suggested that ginsenoside Rh2 could suppress RANKL-induced osteoclast differentiation in vitro and in vivo through the regulation of c-Fos and NFATc1 expressions, not excluding the involvement of NF-κB and ERK. Ginsenoside Rh2 is also suggested to be developed as a therapeutic drug for prevention and treatment of osteoporosis.

Authors+Show Affiliations

Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongwon, South Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22484180

Citation

He, Long, et al. "Ginsenoside Rh2 Inhibits Osteoclastogenesis Through Down-regulation of NF-κB, NFATc1 and C-Fos." Bone, vol. 50, no. 6, 2012, pp. 1207-13.
He L, Lee J, Jang JH, et al. Ginsenoside Rh2 inhibits osteoclastogenesis through down-regulation of NF-κB, NFATc1 and c-Fos. Bone. 2012;50(6):1207-13.
He, L., Lee, J., Jang, J. H., Lee, S. H., Nan, M. H., Oh, B. C., Lee, S. G., Kim, H. H., Soung, N. K., Ahn, J. S., & Kim, B. Y. (2012). Ginsenoside Rh2 inhibits osteoclastogenesis through down-regulation of NF-κB, NFATc1 and c-Fos. Bone, 50(6), 1207-13. https://doi.org/10.1016/j.bone.2012.03.022
He L, et al. Ginsenoside Rh2 Inhibits Osteoclastogenesis Through Down-regulation of NF-κB, NFATc1 and C-Fos. Bone. 2012;50(6):1207-13. PubMed PMID: 22484180.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ginsenoside Rh2 inhibits osteoclastogenesis through down-regulation of NF-κB, NFATc1 and c-Fos. AU - He,Long, AU - Lee,Junwon, AU - Jang,Jae Hyuk, AU - Lee,Sung-Hoon, AU - Nan,Mei Hua, AU - Oh,Byung-Chul, AU - Lee,Sang Gu, AU - Kim,Hong Hee, AU - Soung,Nak Kyun, AU - Ahn,Jong Seog, AU - Kim,Bo Yeon, Y1 - 2012/03/28/ PY - 2012/01/21/received PY - 2012/03/12/revised PY - 2012/03/17/accepted PY - 2012/4/10/entrez PY - 2012/4/10/pubmed PY - 2012/9/14/medline SP - 1207 EP - 13 JF - Bone JO - Bone VL - 50 IS - 6 N2 - Ginsenoside Rh2 is one of the most active components of red ginseng, controlling cancer and other metabolic diseases including osteoclast differentiation. However, the molecular mechanism underlying the inhibition of osteoclast differentiation by ginsenoside Rh2 remains poorly understood. In the present study, it was found that ginsenoside Rh2 suppressed osteoclast differentiation from bone marrow macrophages (BMMs) treated with receptor activator of nuclear factor κB ligand (RANKL) without any cytotoxicity. Ginsenoside Rh2 significantly reduced RANKL-induced expression of transcription factors, c-Fos and nuclear factor of activated T-cells (NFATc1), as well as osteoclast markers, TRAP and OSCAR. In defining the signaling pathways, ginsenoside Rh2 was shown to moderately inhibit NF-κB activation and ERK phosphorylation in response to RANKL stimulation in BMM cells without any effect on p38 and c-Jun N-terminal kinase (JNK). Finally, ginsenoside Rh2 blocked osteoporosis in vivo as confirmed by restored bone mineral density (BMD) and other markers associated osteoclast differentiation. Hence, it is suggested that ginsenoside Rh2 could suppress RANKL-induced osteoclast differentiation in vitro and in vivo through the regulation of c-Fos and NFATc1 expressions, not excluding the involvement of NF-κB and ERK. Ginsenoside Rh2 is also suggested to be developed as a therapeutic drug for prevention and treatment of osteoporosis. SN - 1873-2763 UR - https://www.unboundmedicine.com/medline/citation/22484180/Ginsenoside_Rh2_inhibits_osteoclastogenesis_through_down_regulation_of_NF_κB_NFATc1_and_c_Fos_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S8756-3282(12)00740-5 DB - PRIME DP - Unbound Medicine ER -