Inflammation Research

, 60:1005

Honokiol protects osteoblastic MC3T3-E1 cells against antimycin A-induced cytotoxicity

Authors

    • Department of Food and Nutrition, Education Graduate SchoolKyung Hee University
Original Research Paper

DOI: 10.1007/s00011-011-0360-3

Cite this article as:
Choi, E.M. Inflamm. Res. (2011) 60: 1005. doi:10.1007/s00011-011-0360-3

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.

Keywords

HonokiolMitochondrial dysfunctionMC3T3-E1 cellsOxidative stressPI3K/CREB

Copyright information

© Springer Basel AG 2011