Premium
Deoxyactein Isolated from Cimicifuga racemosa protects osteoblastic MC3T3‐E1 cells against antimycin A‐induced cytotoxicity
Author(s) -
Choi Eun Mi
Publication year - 2013
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.1784
Subject(s) - antimycin a , oxidative stress , chemistry , mitochondrion , microbiology and biotechnology , intracellular , protein kinase b , biochemistry , pharmacology , biology , apoptosis
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. Copyright © 2011 John Wiley & Sons, Ltd.