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Exposure of MC3T3\u2010E1 cells to antimycin A caused significant cell viability loss, as well as mitochondrial membrane potential dissipation, complex IV inactivation, ATP loss, intracellular calcium ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) elevation and oxidative stress. Pretreatment with deoxyactein prior to antimycin A exposure significantly reduced antimycin A\u2010induced cell damage by preventing mitochondrial membrane potential dissipation, complex IV inactivation, ATP loss, [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> elevation and oxidative stress. Moreover, deoxyactein increased the activation of PI3K (phosphoinositide 3\u2010kinase), Akt (protein kinase B) and CREB (cAMP\u2010response element\u2010binding protein) inhibited by antimycin A. All these data indicate that deoxyactein may reduce or prevent osteoblasts degeneration in osteoporosis or other degenerative disorders. 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