Ginsenoside Rh2 inhibits osteoclastogenesis through down-regulation of NF-kappaB, NFATc1 and c-Fos

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Title
Ginsenoside Rh2 inhibits osteoclastogenesis through down-regulation of NF-kappaB, NFATc1 and c-Fos
Author(s)
Long He; J Lee; Jae-Hyuk Jang; S H Lee; M H Nan; B C Oh; Sangku Lee; H H Kim; Nak Kyun SoungJong Seog AhnBo Yeon Kim
Bibliographic Citation
Bone, vol. 50, no. 6, pp. 1207-1213
Publication Year
2012
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.
Keyword
Ginsenoside Rh2NF-κBNFATc1OsteoclastOsteoporosis
ISSN
8756-3282
Publisher
Elsevier
DOI
http://dx.doi.org/10.1016/j.bone.2012.03.022
Type
Article
Appears in Collections:
Ochang Branch Institute > Anticancer Agent Research Center > 1. Journal Articles
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