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Glucocorticoid osteoporosis is the most common secondary osteoporosis, pathological fractures resulting often delayed union or nonunion , high morbidity , is a worldwide problem in the orthopedic field . Currently the disease pathogenesis is unclear , there is no effective treatment . Therefore, the research on how to prevent glucocorticoid osteoporosis has very important significance. The study included experiments in vitro and in vivo animal experiments in two parts, a nitric oxide (nitric oxide, NO) in glucocorticoid osteoporosis pathogenesis and the role of simvastatin on NO and glucocorticoid regulation steroid-induced osteoporosis prevention. Materials and Methods 1 . Vitro experiments from neonatal SD rat calvaria osteoblasts were isolated and cultured , were randomly divided into A, B, C three groups of eight , A group added 10 -7 mol / L dexamethasone , 10 -7 mol / L of simvastatin and 0.1 % dimethyl sulfoxide solvent : B group join 10 -7 mol / L dexamethasone and 0.1 % dimethyl sulfoxide ; C group, an increase of only 0.1% DMSO as a control. After 96 hours , using Trizol Reagent kit to extract osteoblast RNA; application -step RT-PCR analysis of endothelial nitric oxide synthase (endothelial nitric oxide synthase, eNOS) mRNA and osteocalcin mRNA expression ; using MTT Determination of cell proliferation rate , measured by nitrate reductase in the cell culture medium NO content . 2 In vivo animal experiments from healthy 6 -month-old male SD rats were randomly divided into three groups: experimental group, model group and the control group 12 . Experimental group once daily gavage method simvastatin 10mg/kg,
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