caa a22 4500 445886161 CHVBK 20180317145600.0 cr unu---uuuuu 170323e20111101xx s 000 0 eng 10.1007/s00011-011-0360-3 doi (NATIONALLICENCE)springer-10.1007/s00011-011-0360-3 Choi Eun Department of Food and Nutrition, Education Graduate School, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, 130-701, Seoul, Korea aut Honokiol protects osteoblastic MC3T3-E1 cells against antimycin A-induced cytotoxicity [Elektronische Daten] [Eun Choi] 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. Springer Basel AG, 2011 Honokiol nationallicence Mitochondrial dysfunction nationallicence MC3T3-E1 cells nationallicence Oxidative stress nationallicence PI3K/CREB nationallicence Inflammation Research SP Birkhäuser Verlag Basel 60/11(2011-11-01), 1005-1012 1023-3830 60:11<1005 2011 60 11 https://doi.org/10.1007/s00011-011-0360-3 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00011-011-0360-3 text/html Onlinezugriff via DOI NATIONALLICENCE 100 1- Choi Eun Department of Food and Nutrition, Education Graduate School, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, 130-701, Seoul, Korea aut NATIONALLICENCE 773 0- Inflammation Research SP Birkhäuser Verlag Basel 60/11(2011-11-01), 1005-1012 1023-3830 60:11<1005 2011 60 11 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer