Protective effect of albiflorin against oxidative-stress-mediated toxicity in osteoblast-like MC3T3-E1 cells |
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| Institution: | 1. Research Institute of Endocrinology, Kyung Hee University Hospital, 1, Hoegi-dong, Dongdaemun-gu, Seoul 130-702, Republic of Korea;2. Department of Food & Nutrition, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea;3. Department of Endocrinology & Metabolism, School of Medicine, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea;1. Department of Clinical Laboratory, Yantai Affiliated Hospital of Binzhou Medical University, Yantai 264100, PR China;2. Center of Translational Medicine, Zibo Central Hospital Affiliated to Shandong University, 54 Gongqingtuan Xi Road, Zibo 255036, PR China;1. Molecular Oncology and Viral Pathology Group, IPO-Porto Research Centre (CI-IPOP), Porto, Portugal;2. Faculty of Medicine, University of Porto, Porto, Portugal;3. LPCC Research Department, Portuguese League Against Cancer (NRNorte), Porto, Portugal;4. Oncology Research Group, UMIB—Unit for Multidisciplinary Research in Biomedicine, Porto, Portugal;5. University of Maryland Marlene and Stewart Greenebaum Comprehensive Cancer Center, Antwerp University Hospital, Edegem, Belgium;6. Centre of Oncological Research (CORE), Antwerp University, Edegem, Belgium;7. Department of Medical Oncology, Centro Hospitalar do Porto, Porto, Portugal;8. ICBAS-UP—Instituto de Ciências Biomédicas Abel Salazar, University of Porto, Porto, Portugal |
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| Abstract: | Albiflorin isolated from Paeoniae Radix was investigated for its ability to protect against antimycin A-induced osteoblast toxicity in the MC3T3-E1 cell line. MC3T3-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. |
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