Journal
FITOTERAPIA
Volume 89, Issue -, Pages 33-41Publisher
ELSEVIER
DOI: 10.1016/j.fitote.2013.05.016
Keywords
Albiflorin; Mitochondrial dysfunction; Osteoblastic MC3T3-E1 cells
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Funding
- Basic Science Research Program through the National Research Foundation of Korea (NRF)
- Ministry of Education, Science and Technology [2012-0002531]
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Albiflorin isolated from Paeoniae Radix was investigated for its ability to protect against antimycin A-induced osteoblast toxicity in the MC3T3-E1 cell line. MCT3-E1 cells showed significantly reduced viability, increased apoptosis and lactate dehydrogenase release, elevated ROS/RNS levels, and decreased mitochondrial function after exposure to antimycin A. Pretreatment with albiflorin reversed the loss of cell viability in antimycin A-treated cultures. Similarly, pretreatment with albiflorin before antimycin A resulted in decreased apoptosis and lactate dehydrogenase release, decreased ROS/RNS levels, and increased mitochondrial function compared to antimycin A-treated cultures. In addition, albiflorin increased the mineralization reduced by antimycin A. Albiflorin reduced antimycin A-induced mitochondrial cytochrome c loss and cardiolipin peroxidation, conferring protection against ROS. These results confirmed the crucial role of cytochrome c and cardiolipin in the underlying mechanistic action of albiflorin. Therefore, the results suggest that albiflorin enhances mitochondrial function to suppress antimycin A-induced oxidative damage via the preservation of cytochrome c and cardiolipin. All of these data indicate that albiflorin may reduce or prevent osteoblast degeneration in osteoporosis. (c) 2013 Elsevier B.V. All rights reserved.
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