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- W3032752012 abstract "ObjectiveTo observe the changes in bone mineral density and microstructure parameters in sclerostin (SOST) gene knockout mice treated with glucocorticoid.Methods12 4-week-old SOST knockout mice were randomly divided into two groups (n=6): methylprednisolone intervention group [SOM group, methylprednisolone 3 mg/(kg·d), subcutaneous injection], placebo group (SOS group, isovolumetric saline subcutaneous injection). 12 wild-type mice were randomly divided into two groups (n=6): wild-type placebo group (WTS group, isovolumetric saline subcutaneous injection), wild methylprednisolone intervention group [WTM group, methylprednisolone 3 mg/(kg·d), subcutaneous injection]. 12 weeks later, mice were sacrificed and one lumbar vertebra of each mouse was selected for micro-CT analysis.ResultsThere was no difference in bone mineral density (BMD), trabecular volume fraction, trabecular number and trabecular thickness between SOM and SOS groups (P>0.05). BMD, trabecular volume fraction, trabecular number and trabecular thickness in SOM and SOS groups were significantly higher than those in WTS and WTM groups (P<0.05). BMD, trabecular volume fraction, trabecular number and trabecular thickness in WTM group were significantly lower than those in WTS group (P<0.05).ConclusionsSclerotin gene knockout mice can resist glucocorticoid-induced bone loss and bone microarchitectural deterioeration. The treatment of osteoporosis with SOST/sclerotin as a target will be an effective method in the future.Key words: Glucocorticoids; Sclerotin; Gene knockout techniques; Bone density; Mice" @default.
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- W3032752012 date "2019-11-20" @default.
- W3032752012 modified "2023-09-26" @default.
- W3032752012 title "Resistance of osteosclerotin knockout mice to glucocorticoid induced bone microstructure degeneration" @default.
- W3032752012 doi "https://doi.org/10.3760/cma.j.issn.1008-1372.2019.11.008" @default.
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