3-nitrotyrosine and 23-epi-26-deoxyactein

Deoxyactein is one of the major constituents isolated from Cimicifuga racemosa. In the present study, we investigated the protective effects of deoxyactein on antimycin A (mitochondrial electron transport inhibitor)-induced toxicity in osteoblastic MC3T3-E1 cells. Exposure of MC3T3-E1 cells to antimycin A caused significant cell viability loss, as well as mitochondrial membrane potential dissipation, complex IV inactivation, ATP loss, intracellular calcium ([Ca(2+) ]i ) elevation and oxidative stress. Pretreatment with deoxyactein prior to antimycin A exposure significantly reduced antimycin A-induced cell damage by preventing mitochondrial membrane potential dissipation, complex IV inactivation, ATP loss, [Ca(2+) ]i elevation and oxidative stress. Moreover, deoxyactein increased the activation of PI3K (phosphoinositide 3-kinase), Akt (protein kinase B) and CREB (cAMP-response element-binding protein) inhibited by antimycin A. All these data indicate that deoxyactein may reduce or prevent osteoblasts degeneration in osteoporosis or other degenerative disorders.

Topics: 3T3 Cells; Adenosine Triphosphate; Animals; Antifungal Agents; Antimycin A; Calcium; Cardiolipins; Cimicifuga; Coloring Agents; Cyclic AMP Response Element-Binding Protein; Electron Transport Complex IV; Membrane Potential, Mitochondrial; Mice; Mitochondria; Oncogene Protein v-akt; Osteoblasts; Oxidation-Reduction; Oxidative Stress; Phosphatidylinositol 3-Kinases; Saponins; Tetrazolium Salts; Thiazoles; Thioredoxin-Disulfide Reductase; Triterpenes; Tyrosine