期刊
JOURNAL OF APPLIED TOXICOLOGY
卷 33, 期 6, 页码 488-494出版社
WILEY
DOI: 10.1002/jat.1784
关键词
deoxyactein; mitochondrial dysfunction; MC3T3-E1 cells; oxidative stress; PI3K; Akt; CREB
类别
资金
- Basic Science Research Program through the National Research Foundation of Korea
- Ministry of Education, Science and Technology [20110005020]
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 ([Ca2+]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, [Ca2+]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 (c) 2011 John Wiley & Sons, Ltd.
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