Background Estrogen deficiency results in loss of bone mass compounds with estrogen-like activity that bind to estrogen receptors effect of the phytoestrogen puerarin on adult mouse osteoblasts. Methods Osteoblast cel...Background Estrogen deficiency results in loss of bone mass compounds with estrogen-like activity that bind to estrogen receptors effect of the phytoestrogen puerarin on adult mouse osteoblasts. Methods Osteoblast cells were harvested from 8-month old female Phytoestrogens are plant-derived non-steroidal The main aim of this study was to investigate the mprinting control region （ICR） mice. The effects of puerarin stimulation on the proliferation, differentiation and maturation of osteoblasts were examined. The production of nitric oxide （NO） and the expression of bone morphogenetic protein-2 （BMP-2）, SMAD4, mitogen-activated protein kinases （MAPK）, core binding factor all runt-related transcription factor 2 （Cbfal/Runx2）, osteoprotegerin （OPG）, and receptor activator of NF-KB ligand （RANKL） genes were analyzed. The activation of signal pathways was further confirmed by specific pathway inhibitors. Results The osteoblast viability reached its maximum at 10-8 mol/L puerarin. At this concentration, puerarin increases the proliferation and matrix mineralization of osteoblasts and promotes NO synthesis. With 108 mol/L puerarin treatment, BMP-2, SMAD4, Cbfal/Runx2, and OPG gene expression were up-regulated, while the RANKL gene expression is down-regulated. Concurrent treatment involving the （bone morphogenetic protein） BMP antagonist Noggin or the NOS inhibitor L-NAME diminishes puerarin induced cell proliferation, Alkaline phosphatase （ALP） activity, NO production, as well as the BMP-2, SMAD4, Cbfal/Runx2, OPG, and RANKL gene expression. Conclusions In this in vitro study, we demonstrate that puerarin is a bone anabolic agent that exerts its osteogenic effects through the induction of BMP-2 and NO synthesis, subsequently regulating Cbfal/Runx2, OPG, and RANKL gene expression. This effect may contribute to its induction of osteoblast proliferation and differentiation, resulting in bone formation.展开更多
文摘Background Estrogen deficiency results in loss of bone mass compounds with estrogen-like activity that bind to estrogen receptors effect of the phytoestrogen puerarin on adult mouse osteoblasts. Methods Osteoblast cells were harvested from 8-month old female Phytoestrogens are plant-derived non-steroidal The main aim of this study was to investigate the mprinting control region （ICR） mice. The effects of puerarin stimulation on the proliferation, differentiation and maturation of osteoblasts were examined. The production of nitric oxide （NO） and the expression of bone morphogenetic protein-2 （BMP-2）, SMAD4, mitogen-activated protein kinases （MAPK）, core binding factor all runt-related transcription factor 2 （Cbfal/Runx2）, osteoprotegerin （OPG）, and receptor activator of NF-KB ligand （RANKL） genes were analyzed. The activation of signal pathways was further confirmed by specific pathway inhibitors. Results The osteoblast viability reached its maximum at 10-8 mol/L puerarin. At this concentration, puerarin increases the proliferation and matrix mineralization of osteoblasts and promotes NO synthesis. With 108 mol/L puerarin treatment, BMP-2, SMAD4, Cbfal/Runx2, and OPG gene expression were up-regulated, while the RANKL gene expression is down-regulated. Concurrent treatment involving the （bone morphogenetic protein） BMP antagonist Noggin or the NOS inhibitor L-NAME diminishes puerarin induced cell proliferation, Alkaline phosphatase （ALP） activity, NO production, as well as the BMP-2, SMAD4, Cbfal/Runx2, OPG, and RANKL gene expression. Conclusions In this in vitro study, we demonstrate that puerarin is a bone anabolic agent that exerts its osteogenic effects through the induction of BMP-2 and NO synthesis, subsequently regulating Cbfal/Runx2, OPG, and RANKL gene expression. This effect may contribute to its induction of osteoblast proliferation and differentiation, resulting in bone formation.
