Abstract
Osteonecrosis of the femoral head (ONFH) can be caused by a decrease in the activity or numbers of osteoblasts, a process in which apoptosis may play an essential role. We investigated the effect of dexamethasone (Dex) combined with hypoxic stress on murine osteoblastic MC3T3-E1 cells. Flow cytometry, western blot and real-time quantitative PCR analyses revealed that hypoxia significantly enhanced Dex-induced apoptosis. Further data demonstrated that both the death receptor and the mitochondria-mediated pathway were involved in Dex-induced apoptosis under hypoxic conditions. However, the death receptor pathway had only a minor effect on this process. The expression levels of Bcl-2 and Bax, which regulate the mitochondria-initiated apoptotic cascade signaling pathway, were significantly different in response to Dex and hypoxia. The mitochondrial membrane potential collapsed, and the inhibitor brain- derived neurotrophic factor (BDNF) conferred effective protection against apoptosis. In summary, the mitochondria-mediated apoptotic pathway functions in osteoblast apoptosis that is induced by Dex in a hypoxic environment, and the present study may help us to gain further insight into the molecular mechanisms of steroid-induced ONFH.
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