期刊
JOURNAL OF MEDICINAL FOOD
卷 17, 期 4, 页码 414-423出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/jmf.2013.2841
关键词
actein; CREB; differentiation; mitochondrial dysfunction; MC3T3-E1 cells; oxidative stress
资金
- National Research Foundation of Korea (NRF) - Ministry of Education [NRF-2013R1A1A2A10004361]
Actein, isolated fromblack cohosh, was subjected to in vitro experiments to investigate its functional bioactivities in osteoblastic MC3T3-E1 cells. Actein caused a significant elevation of alkaline phosphatase activity, collagen synthesis, osteocalcin production, mineralization, and glutathione content in the cells, suggesting that actein has a stimulatory effect on osteoblastic bone formation or has potential activity against osteoporosis. We investigated the protective effects of actein on mitochondrial electron transport inhibitor, antimycin A induced toxicity in osteoblastic MC3T3-E1 cells. Exposure of MC3T3-E1 cells to antimycin A caused significant decrease in cell viability and mineralization. However, pretreatment with actein prior to antimycin A exposure significantly reduced antimycin A-induced cell damage by preventing mitochondrial membrane potential dissipation, complex IVinactivation, cardiolipin oxidation, ROS release, and nitrotyrosine increase, suggesting that actein may be useful for protecting mitochondria against a burst of oxidative stress. In addition, actein increased the phosphorylation of CREB (cAMP-response element-binding protein) inhibited by antimycin A and decreased the production of TNF-alpha induced by antimycin A. These findings suggest that actein could prevent oxidative damage to osteoblasts in osteoporotic patients.
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