Ginsenoside Rb1 inhibits osteoclastogenesis by modulating NF-κB and MAPKs pathways

Binbin Cheng, Jun Li, Juan Du, Xiang Lv, Li Weng, Changquan Ling
Food and Chemical Toxicology 2012, 50 (5): 1610-5
Ginsenosides (GSS), the main active components of ginseng, have been reported possessing anti-osteoporosis activity in ovariectomized rats. However, the active ingredient and the mechanisms underlying the anti-osteoporosis activity of GSS have not been clearly elucidated. In the present study, we determined the effect of ginsenoside Rb1, a major component of ginsenosides, on receptor activator of NF-κB ligand (RANKL)-induced osteoclast formation. Ginsenoside Rb1 inhibited RANKL-induced osteoclast differentiation from Raw264.7 cells without cytotoxicity. Ginsenoside Rb1 also inhibited RANKL-induced TNFα mRNA expression in Raw264.7 cells. Pretreatment with ginsenoside Rb1 significantly inhibited RANKL-induced the gene expression of c-Fos and nuclear factor of activated T-cells c1 (NFATc1), which are two essential and crucial transcription factors for osteoclast formation. Rb1 inhibited RANKL-induced nucleus translocation and activation of NF-κB, the upstream factor of c-Fos and NFATc1. Among the three well known mitogen-activated protein kinases (MAPKs), Rb1 inhibited RANKL-induced JNK and p38 phosphorylation, but not ERK1/2. Taken together, our data suggest that ginsenoside Rb1 is one of the effective components of GSS for the anti-osteoporosis activity and can inhibit osteoclastogenesis by suppressing RANKL-induced activation of both JNK and p38 MAPKs and NF-κB pathways, and consequently down-regulating the gene expression of c-Fos and NFATc1 in osteoclast precursors.

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