Eun Mi Choi1. 1. Department of Food and Nutrition, Education Graduate School, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, Seoul, 130-701, Korea. cheunmi@hanmail.net
Abstract
OBJECTIVE: Honokiol is a phenolic compound isolated from the bark of Magnolia officinalis, a plant widely used in traditional medicine. Antimycin A, which inhibits complex III of the electron transport system, has been used as a reactive oxygen species generator in biological systems. In the present study, we investigated the protective effects of honokiol on antimycin A-induced dysfunction in osteoblastic MC3T3-E1 cells. MATERIALS AND METHODS: Osteoblastic MC3T3-E1 cells were pre-incubated with honokiol before treatment with antimycin A, and markers of mitochondrial function and oxidative damage were examined. In addition, the effects of honokiol on the activation of PI3K (phosphoinositide 3-kinase) and CREB (cAMP-responsive element-binding protein) were examined in MC3T3-E1 cells. RESULTS: Honokiol significantly (P < 0.05) increased cell viability and calcium deposition and decreased the production of ROS in the presence of antimycin A. Moreover, pretreatment with honokiol prior to antimycin A exposure significantly reduced antimycin A-induced mitochondrial membrane potential (MMP) dissipation, complex IV inactivation, nitrotyrosine formation, and thioredoxin reductase inactivation. Honokiol also induced the activation of PI3K and CREB inhibited by antimycin A, which demonstrates that honokiol utilizes the PI3K and CREB pathway to augment metabolic activity inhibited by antimycin A. CONCLUSION: Honokiol may reduce or prevent osteoblast degeneration in osteoporosis or other degenerative disorders.
OBJECTIVE:Honokiol is a phenolic compound isolated from the bark of Magnolia officinalis, a plant widely used in traditional medicine. Antimycin A, which inhibits complex III of the electron transport system, has been used as a reactive oxygen species generator in biological systems. In the present study, we investigated the protective effects of honokiol on antimycin A-induced dysfunction in osteoblastic MC3T3-E1 cells. MATERIALS AND METHODS: Osteoblastic MC3T3-E1 cells were pre-incubated with honokiol before treatment with antimycin A, and markers of mitochondrial function and oxidative damage were examined. In addition, the effects of honokiol on the activation of PI3K (phosphoinositide 3-kinase) and CREB (cAMP-responsive element-binding protein) were examined in MC3T3-E1 cells. RESULTS:Honokiol significantly (P < 0.05) increased cell viability and calcium deposition and decreased the production of ROS in the presence of antimycin A. Moreover, pretreatment with honokiol prior to antimycin A exposure significantly reduced antimycin A-induced mitochondrial membrane potential (MMP) dissipation, complex IV inactivation, nitrotyrosine formation, and thioredoxin reductase inactivation. Honokiol also induced the activation of PI3K and CREB inhibited by antimycin A, which demonstrates that honokiol utilizes the PI3K and CREB pathway to augment metabolic activity inhibited by antimycin A. CONCLUSION:Honokiol may reduce or prevent osteoblast degeneration in osteoporosis or other degenerative disorders.