prevent bone loss in ovariectomized rats and orchidectomized rats; inhibit osteoclastic differentiation and bone resorption by increasing the activity of mature osteoblasts via ERβ, regulating RUNX 2/Cbfα1 production, and stimulating the secretion osteoprotegerin.
increase ALP activity in cultured human MG-63 osteoblasts through ERK and ER pathway; prevent antimycin A-induced cell damage in mitochondrial membrane potential dissipation, complex IV inactivation, ROS production through activation of PI3K (phosphoinositide 3-kinase), Akt (protein kinase B), CREB (cAMP-response element-binding protein) in MC3T3-E1.
reverse the decreased biomechanical quality and the impaired microarchitecture of the femurs in diabetic rats through improving antioxidant capacity; inhibit osteoclastic differentiation and bone resorption via inducing apoptosis and involving NF-B and AP-1.
protect against retinoic acid-induced osteoporosis and improve bone quality in rats; perturb osteoclast formation and bone resorption by inhibiting RANK-mediated NF-B and ERK signaling; induce bone morphogenetic protein-2 expression via PI3K, Akt, c-Fos/c-Jun and AP-1 pathway in osteoblasts; prevent hydrogen peroxide-induced dysfunction in osteoblastic MC3T3-E1 cells.
protect osteoblasts against hydrogen peroxide-induced osteoblastic dysfunction, exert antiresorptive actions via the reduction of RANKL and oxidative damage
prevent bone loss in ovariectomized rats; suppress formation and bone resorption of osteoclast induced by interleukin-1; suppress the expression of cyclooxygenase-2, NF-κB-dependent transcription, and prostaglandin E production in osteoblasts.
increase bone mineral density and bone mineral content of trabecular and cortical bones in the femur of OVX rats; inhibit the differentiation of both bone marrow mononuclear cells and RAW 264.7 cells into osteoclasts and the bone resorptive activity of osteoclasts.
inhibit the differentiation and bone resorptive activity of osteoclasts by inhibiting RANKL-induced activation of signaling molecules (Akt, ERK/MAP kinase and NF-B) and mRNA expression of osteoclast-associated genes TRAP, matrix metalloproteinase 9 and c-Src, c-Fos, Fra-2 and NFATc1.
upregulate ALP activity and expression of osteogenic marker genes by activation of RUNX2 via mechanisms related to the p38 MAPK and ERK signaling pathway
prevent bone loss and improve bone microarchitecture, histomorphometric parameters, and biomechanical properties in OVX rats; stimulate osteoblast proliferation and differentiation through β-catenin/BMP signaling.
increase cell growth, alkaline phosphatase activity, collagen synthesis, mineralization, glutathione content, and osteoprotegerin release in the osteoblast; decrease the production of TNF-α, IL-6, and RANKL in the presence of antimycin A; stimulate osteoblastogenesis by suppressing NF-κB activation.
improve bone mineral content, bone mineral density, and bone strength indexes in OVX control rats; slightly increase bone formation and significantly inhibit bone resorption
cause a significant elevation of cell growth, alkaline phosphatase activity, collagen synthesis, mineralization, and glutathione content in osteoblast; decrease the production of osteoclast differentiation inducing factors such as RANKL, TNF-α, and IL-6 in the presence of antimycin A
prevent osteoporosis induced by cyclosporin A; inhibit the differentiation and bone resorbing activity of osteoclasts through inhibition of ROS production; promote the formation of osteoblasts by induction of bone morphogenetic protein-2 through Src kinase-dependent estrogen receptor activation; promote osteogenesis of human mesenchymal stem cells by upregulating RUNX2 gene expression via the SIRT1/FOXO3A axis.
improve bone microarchitecture and mineral density in APP/PS1 transgenic mice; improve bone strength and biochemical marker in ovariectomized mature rat model; inhibit OVX-induced bone loss by reducing osteoclastogenesis through increasing antioxidant activity and impairing RANKL signaling.
attenuate trabecular and cortical bone loss through increasing bone formation while suppressing bone resorption due to its antioxidant capacity; inhibit the formation and differentiation of osteoclasts via inhibition of matrix metalloproteinases.
decrease bone resorption, the number of multinucleated osteoclasts, and the activity TRAP and cathepsin K of osteoclast; induce the apoptosis of osteoclasts through improving the ratio of OPG and RANKL in osteoblasts, interfering with the JNK and NF-κB signal pathway, and reducing the expression of calcitonin receptor and carbonic anhydrase/II in osteoclasts.
prevent bone loss in ovariectomized osteoporosis model mice; inhibit osteoclast formation and bone resorption via downregulation of c-Fos and NFATc1 induced by RANKL.
inhibit RANKL-induced NF-B phosphorylation in osteoclast precursors; suppress the formation, differentiation and bone resorption of osteoclast through regulation of RANKL and OPG gene expression in osteoblastic cells
inhibit osteoclast formation and bone resorption in the co-culture system with mouse bone marrow cells (BMC) and osteoblasts; induce disruption of actin ring formation in mature osteoclasts with an impact on cell viability
prevent bone loss in SAMP6 senile osteoporosis model and ovariectomized rats; inhibit formation and differentiation of osteoclast; promote osteoblast differentiation through activation of Runx2 by p38 MAPK.
inhibit bone loss in ovariectomized mice; promote the proliferation and differentiation of osteoblast; prevent hydrogen peroxide-induced dysfunction and oxidative damage in calvarial osteoblasts; inhibit the formation, differentiation and bone resorption of osteoclast.
reduce oxidative stress and the levels of bone turnover markers in postmenopausal women; stimulate proliferation and alkaline phosphatase activity of osteoblasts; inhibit osteoclasts formation and bone resorption activity.
prevent bone loss from long-term administration of prednisone in rats; protect bone from glucocorticoid—induced bone marrow impairment by stimulating osteogenesis and depressing adipogenesis in bone marrow stromal cells.
prevent glucocorticoid—induced cancellous bone loss and decrease adipogenesis; stimulate bone marrow stromal cell differentiation to osteoblast and increase osteoblast activities; decrease glucocorticoid—induced associated adipogenic differentiation through regulating the mRNA expression of PPAR-γ, Runx2, Dickkopf-1 and β-catenin in MSC
prevent bone loss in mice; inhibit osteoclastogenesis by inhibiting the phosphorylation of JNK, and expression of NFATc1 and c-Fos; suppresses 2-methylene-19-nor-(20S)-1α, 25(OH)2D3—induced hypercalcemia as resulting from the inhibition of osteoclastogenesis
