title: Deoxyactein Isolated from Cimicifuga racemosa protects osteoblastic MC3T3-E1 cells against antimycin A-induced cytotoxicity.
abstract: 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.
authors.affiliation: Department of Food and Nutrition, Education Graduate School, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, Seoul, 130-701, Korea. cheunmi@hanmail.net
authors.forename: Eun Mi
authors.initials: EM
authors.lastname: Choi
mesh_terms: D016475:3T3 Cells; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D000935:Antifungal Agents / Q000037:antagonists & inhibitors* / Q000633:toxicity; D000968:Antimycin A / Q000037:antagonists & inhibitors* / Q000633:toxicity; D002118:Calcium / Q000378:metabolism; D002308:Cardiolipins / Q000378:metabolism; D031885:Cimicifuga / Q000737:chemistry*; D004396:Coloring Agents; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism; D003576:Electron Transport Complex IV / Q000378:metabolism; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D051379:Mice; D008928:Mitochondria / Q000187:drug effects; D051058:Oncogene Protein v-akt / Q000378:metabolism; D010006:Osteoblasts / Q000187:drug effects*; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D012503:Saponins / Q000302:isolation & purification / Q000494:pharmacology*; D013778:Tetrazolium Salts; D013844:Thiazoles; D013880:Thioredoxin-Disulfide Reductase / Q000378:metabolism; D014315:Triterpenes / Q000302:isolation & purification / Q000494:pharmacology*; D014443:Tyrosine / Q000031:analogs & derivatives / Q000378:metabolism
chemical_list: D000935:Antifungal Agents; D002308:Cardiolipins; D004396:Coloring Agents; D017362:Cyclic AMP Response Element-Binding Protein; D012503:Saponins; D013778:Tetrazolium Salts; D013844:Thiazoles; D014315:Triterpenes; C457248:23-epi-26-deoxyactein; C002744:3-nitrotyrosine; D014443:Tyrosine; D000968:Antimycin A; D000255:Adenosine Triphosphate; D013880:Thioredoxin-Disulfide Reductase; D003576:Electron Transport Complex IV; D019869:Phosphatidylinositol 3-Kinases; D051058:Oncogene Protein v-akt; C022616:thiazolyl blue; D002118:Calcium