| Objective To investigate the effect of dexamethasone (Dex) induced apoptosis of osteoblasts in vitro and to explore the molecular mechanism of dexamethasone in the apoptosis of osteoblasts. Methods Different concentrations of dexamethasone (10-8 mol/L, 10-6 mol/L, 10-4mol/L) were used in the isolated osteoblasts of SD rats. The nucleus morphology was observed by DAPI staining. The morphology of nuclei and mitochondria was observed by transmission electron microscopy. The apoptosis rate of osteoblasts was detected by flow cytometry, and the mitochondrial transmembrane potential was detected by JC-1 fluorescence probe. Results After intervention for 24 hours using 10-8 mol/L, 10-6 mol/L, and 10-4mol/L dexamethasone, DAPI staining showed that the osteoblasts of 10-8mol/L dexamethasone group were rarely apoptotic, and the apoptosis of osteoblasts in 10-6mol/L and 10-4mol/L dexamethasone groups was obvious, the higher the concentration of dexamethasone, the more obvious apoptotic phenomena, such as nuclear condensation and nuclear cracking. The transmission electron microscopy showed that with the increase of dexamethasone concentration, the nuclear condensation was obvious, the swelling and vacuolar changes of mitochondria increased. And the apoptosis rate of osteoblasts gradually increased with the increase of dexamethasone concentration. Compared with the blank control group, the apoptosis rate of 10-8mol/L dexamethasone group was not significantly changed (P>0.05). The apoptosis rate of osteoblasts in 10-6 mol/L and 10-4mol/L dexamethasone groups was increased by 7.240% and 31.173% respectively (P<0.05). With the increase of dexamethasone concentration, the mitochondrial membrane potential decreased gradually. Compared with the blank control group, the decrease of the cell membrane potential of 10-8mol/L dexamethasone group was not obvious (P>0.05), The membrane potential of 10-6 mol/L and 10-4mol/L dexamethasone groups decreased by 6.814% and 17.846% respectively (P<0.05). Conclusion Dexamethasone induces apoptosis of osteoblasts through activation of mitochondrial pathway in a concentration dependent manner. |