Eudebeiolide B inhibits osteoclastogenesis and prevents ovariectomy-induced bone loss by regulating RANKL-induced NF-κB, c-Fos and calcium signaling
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- Eudebeiolide B inhibits osteoclastogenesis and prevents ovariectomy-induced bone loss by regulating RANKL-induced NF-κB, c-Fos and calcium signaling
- M H Kim; Hyung Jin Lim; Seong Gyeong Bak; Eun Jae Park; Hyun-Jae Jang; Seung Woong Lee; Soyoung Lee; K M Lee; S H Cheong; Seung Jae Lee; Mun Chual Rho
- Bibliographic Citation
- Pharmaceuticals, vol. 13, no. 12, pp. 468-468
- Publication Year
- Eudebeiolide B is a eudesmane-type sesquiterpenoid compound isolated from Salvia plebeia R. Br., and little is known about its biological activity. In this study, we investigated the effects of eudebeiolide B on osteoblast differentiation, receptor activator nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis in vitro and ovariectomy-induced bone loss in vivo. Eudebeiolide B induced the expression of alkaline phosphatase (ALP) and calcium accumulation during MC3T3-E1 osteoblast differentiation. In mouse bone marrow macrophages (BMMs), eudebeiolide B suppressed RANKL-induced osteoclast differentiation of BMMs and bone resorption. Eudebeiolide B downregulated the expression of nuclear factor of activated T-cells 1 (NFATc1) and c-fos, transcription factors induced by RANKL. Moreover, eudebeiolide B attenuated the RANKL-induced expression of osteoclastogenesis-related genes, including cathepsin K (Ctsk), matrix metalloproteinase 9 (MMP9) and dendrocyte expressed seven transmembrane protein (DC-STAMP). Regarding the molecular mechanism, eudebeiolide B inhibited the phosphorylation of Akt and NF-κB p65. In addition, it downregulated the expression of cAMP response element-binding protein (CREB), Bruton's tyrosine kinase (Btk) and phospholipase Cγ2 (PLCγ2) in RANKL-induced calcium signaling. In an ovariectomized (OVX) mouse model, intragastric injection of eudebeiolide B prevented OVX-induced bone loss, as shown by bone mineral density and contents, microarchitecture parameters and serum levels of bone turnover markers. Eudebeiolide B not only promoted osteoblast differentiation but inhibited RANKL-induced osteoclastogenesis through calcium signaling and prevented OVX-induced bone loss. Therefore, eudebeiolide B may be a new therapeutic agent for osteoclast-related diseases, including osteoporosis, rheumatoid arthritis and periodontitis.
- Eudebeiolide BOsteoporosisRANKLOVX mouse modelCalcium signal
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- Ochang Branch Institute > Division of National Bio-Infrastructure > Bio-Resource Central Bank > 1. Journal Articles
Jeonbuk Branch Institute > Functional Biomaterial Research Center > 1. Journal Articles
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