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Protective effect of apocynin on antimycin A‐induced cell damage in osteoblastic MC3T3 ‐E1 cells
Author(s) -
Choi Eun Mi,
Lee Young Soon
Publication year - 2012
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.1689
Subject(s) - apocynin , chemistry , nadph oxidase , oxidative stress , antimycin a , protein kinase b , chelerythrine , pharmacology , microbiology and biotechnology , kinase , biochemistry , mitochondrion , apoptosis , protein kinase c , biology
Apocynin is a naturally occurring methoxy‐substituted catechol, experimentally used as an inhibitor of NADPH‐oxidase. In the present study, we investigated the protective effects of apocynin on antimycin A (AMA)‐induced toxicicy in osteoblastic MC3T3‐E1 cells. Exposure of MC3T3‐E1 cells to AMA caused significant cell viability loss, as well as mitochondrial membrane potential (MMP) dissipation, complex IV inactivation, ATP loss, intracellular calcium ([Ca 2+ ] i ) elevation and oxidative stress. Pretreatment with apocynin prior to AMA exposure significantly reduced AMA‐induced cell damage by preventing MMP dissipation, complex IV inactivation, ATP loss, [Ca 2+ ] i elevation and oxidative stress. These results suggest that apocynin has a protective effect against AMA‐induced cell damage by its antioxidant effects and the attenuation of mitochondrial dysfunction. Apocynin also induced the activation of PI3K (phosphoinositide 3‐kinase), Akt (protein kinase B) and CREB (cAMP‐response element‐binding protein) inhibited by AMA. All these data indicate that apocynin may reduce or prevent osteoblasts degeneration in osteoporosis or other degenerative disorders. Copyright © 2011 John Wiley & Sons, Ltd.