ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2011
Honokiol protects osteoblastic MC3T3-E1 cells against antimycin A-induced cytotoxicity.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 12 citations in OpenAlex.
- Honokiol, a structurally defined natural product, promotes SIRT3-linked bone formation in osteoporotic bone remodeling and fracture repair.Pharmaceutical biology · 2026Article
- Mitigating mitochondrial dysfunction: a novel strategy for Chinese botanical drugs against osteoporosis.Frontiers in pharmacology · 2026Review
- The Emerging Role of the Mitochondrial Respiratory Chain in Skeletal Aging.Aging and disease · 2024Review
- Potential antiosteoporotic agents from plants: a comprehensive review.Evidence-based complementary and alternative medicine : eCAM · 2012Article
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1 author at 1 institution in 1 country.
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Abstract
objectiveHonokiol 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
methodsOsteoblastic 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.
resultsHonokiol 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.
conclusionHonokiol may reduce or prevent osteoblast degeneration in osteoporosis or other degenerative disorders.
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