Difference investigation of the lumbar bone-loss level induced by prednisolone or dexamethasone and its effects on osteogenic and adipogenic gene expression

English Keywords:Glucocorticoid  Bone mineral density  OPG  PPAR-γ

English Abstract:

  【Abstract】 Objectives: To investigate the mechanism of lumbar bone loss induced by prednisolone(PRE) or dexamethasone(DXM) through the osteogenesis and adipogenesis pathway. Methods: 24 female SD rats aged 3 months was divided into 4 groups randomly as below, baseline group(BL group, 6 rats), age-matched control group(CON group, 6 rats), prednisolone-treated group(PRE group, 6 rats), dexamethasone-treated group(DXM group, 6 rats). BL group were euthanized at the beginning of the experiment and CON group rats were feed normally with no treatment. PRE group and DXM group were injected with PRE in a dose of 5mg/kg per day and DXM in a dose of 1mg/kg twice per week, respectively and lasted for 3 months. The bone marrow in right femur was collected for Oil red staining to observe the cell types, lumbar 6 was collected for testing the activity of osteoprotegerin(OPG) and peroxisome proliferator activated receptor-γ(PPAR-γ) by reverse transcription-polymerase chain reaction(RT-PCR), lumbar 1-3 were collected for BMD at the end of treatment. Results： BMD in PRE and DXM rats were lower than CON rats, and decreased more significantly in DXM rats(P＜0.01). Moreover, DXM rats decreased more significantly compared with PRE rats in BMD. Although the expression level of PPAR-γ had no significant difference among 4 groups， OPG in DXM rats was lower than that in other groups. The amount of red-staining cell in two glucocorticoid treated rats were more than that of BL group, but there was no obvious difference between the treated groups. Conclusions: The effect of DXM on lumbar bone mass decrease is more powerful than that of PRE, which may be caused by restraining the expression of OPG more significantly through OPG/RANKL/RANK pathway.