biostudies-literature00450Unknown18(1)Kim EJBACKGROUND:Schisandra chinenesis (SC) has been reported to have ameliorative effect on osteoporosis. However, the mechanisms underlying the anti-osteoporosis activity of SC have not been clearly elucidated. In the present study, we determined the effects of SC on The receptor activator of NF-kB ligand (RANKL)-induced osteoclastogenesis and its potential mechanism. METHODS:Raw 264.7 cells were treated with 0.6, 6 and 60 ?g/mL SC in the presence of 100 ng/mL RANKL for 7 days. RANKL-induced osteoclast formation was analyzed by tartrate resistant acid phosphatase (TRAP) staining. The osteoclast differentiation-related factors were confirmed along with TNF-?. RESULTS:SC inhibits the RANKL-induced osteoclast differentiation in dose-dependent manner within non-toxic concentrations. The supernatant concentrations of TNF-? were significantly decreased by SC treatment. In addition, osteoclastogenesis-related factors, TRAP6 and NF-?B, were markedly decreased by SC in RANKL-induced osteoclasts. Mechanistically, SC reduced the RANKL-triggered NFATc1 and c-fos expressions. CONCLUSIONS:Taken together, our data suggest that SC can modulate bone metabolism by suppressing RANKL-induced osteoclast differentiation.BMC complementary and alternative medicine270https://www.ebi.ac.uk/biostudies/studies/S-EPMC6167898biostudies-literatureInhibition of RANKL-stimulated osteoclast differentiation by Schisandra chinensis through down-regulation of NFATc1 and c-fos expression.PMC6167898Kim EJKim MHLee HYang WM45falseInhibition of RANKL-stimulated osteoclast differentiation by Schisandra chinensis through down-regulation of NFATc1 and c-fos expression.BACKGROUND:Schisandra chinenesis (SC) has been reported to have ameliorative effect on osteoporosis. However, the mechanisms underlying the anti-osteoporosis activity of SC have not been clearly elucidated. In the present study, we determined the effects of SC on The receptor activator of NF-kB ligand (RANKL)-induced osteoclastogenesis and its potential mechanism. METHODS:Raw 264.7 cells were treated with 0.6, 6 and 60 ?g/mL SC in the presence of 100 ng/mL RANKL for 7 days. RANKL-induced osteoclast formation was analyzed by tartrate resistant acid phosphatase (TRAP) staining. The osteoclast differentiation-related factors were confirmed along with TNF-?. RESULTS:SC inhibits the RANKL-induced osteoclast differentiation in dose-dependent manner within non-toxic concentrations. The supernatant concentrations of TNF-? were significantly decreased by SC treatment. In addition, osteoclastogenesis-related factors, TRAP6 and NF-?B, were markedly decreased by SC in RANKL-induced osteoclasts. Mechanistically, SC reduced the RANKL-triggered NFATc1 and c-fos expressions. CONCLUSIONS:Taken together, our data suggest that SC can modulate bone metabolism by suppressing RANKL-induced osteoclast differentiation.2018-01-01T00:00:00Z2018 Oct2021-02-19T07:30:10Z2019-03-26T23:59:42ZS-EPMC61678983028572210.1186/s12906-018-2331-5