An Experimental Study About The Effect Of Dexamethasone On Mouse Osteoblast Apoptosis And Mechanism

Objective: Observed the impact of different doses of dexametha-sone onosteoblast apoptosis and caspase-3expression; discuss the mechanism ofdexamethasone induced osteoblast apoptosis.Method：⑴Training and save the MC-3T3-E1mouse osteoblast cells.⑵The vigorous growth of MC-3T3-E1Mouse osteoblastic cells were randomlydivided into7groups, The experimental group：the group1-5were treated with10-4-10-8mol/L Dex, The antagonistic group：the group6was treated with10-48mol/L Dex+10-5mol/LRU486， the blank group： without anyintervention.⑶Make the7group cells intervention effect last72hours.Then,detect cell Survival rate and destruction rate by MTT; Application offluorescent dyes Hoechst33258staining of cells was observed number ofapoptotic and morphological; detect the apoptosis rate by FCM(flowcytometry); detect the activity of caspase-3by Microplate reader.Result:1.MTT showed that: With the dexamethasone drug concentrationincreased, the growth inhibition of Dex MC3T3-E1cells were graduallyincreased.2. Fluorescent staining to observe the morphology of apoptosis showedthat: Dexamethasone can promote apoptosis of MC3T3-E1.3.Flow cytometry apoptosis rate showed that: With the increase of theconcentration of dexamethasone,the DNA content of cells gradually decreased,apoptosis increased,and a concentration dependent.4.The ELISA showed that: the caspase-3activity increases expression withDex concentration, the expression was stronger than that to join the GR antagonist group in the same concentration of Dex induced caspase-3activity.Conclusion:1、DEX can promote apoptosis of murine osteoblasts；2、Mouse osteoblast apoptosis rate increased with DEX concentrations increase；3、With the increase of DEX concentration increased caspase-3activity inmouse osteoblastic cells；4、DEX-induced promotion of mouse osteoblastapoptosis through the activation of caspase-3.