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Mol Cell Biochem. 2015 Nov;409(1-2):51-8. doi: 10.1007/s11010-015-2511-2. Epub 2015 Jul 16.

Edaravone protects osteoblastic cells from dexamethasone through inhibiting oxidative stress and mPTP opening.

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Department of Orthopedic and Hand Surgery, Liyuan Hospital, Huazhong University of Science and Technology, Wuhan, China.
Department of Clinical Laboratory, The People's Hospital of Lishui, Lishui, 323000, Zhejiang, China.
Department of Orthopaedics, The People's Hospital of Lishui, Lishui, 323000, Zhejiang, China.


Existing evidences have emphasized an important role of oxidative stress in dexamethasone (Dex)-induced osteoblastic cell damages. Here, we investigated the possible anti-Dex activity of edaravone in osteoblastic cells, and studied the underlying mechanisms. We showed that edaravone dose-dependently attenuated Dex-induced death and apoptosis of established human or murine osteoblastic cells. Further, Dex-mediated damages to primary murine osteoblasts were also alleviated by edaravone. In osteoblastic cells/osteoblasts, Dex induced significant oxidative stresses, tested by increased levels of reactive oxygen species and lipid peroxidation, which were remarkably inhibited by edaravone. Meanwhile, edaravone repressed Dex-induced mitochondrial permeability transition pore (mPTP) opening, or mitochondrial membrane potential reduction, in osteoblastic cells/osteoblasts. Significantly, edaravone-induced osteoblast-protective activity against Dex was alleviated with mPTP inhibition through cyclosporin A or cyclophilin-D siRNA. Together, we demonstrate that edaravone protects osteoblasts from Dex-induced damages probably through inhibiting oxidative stresses and following mPTP opening.


Dexamethasone; Edaravone; Osteoblasts; Osteonecrosis; Oxidative stress

[Indexed for MEDLINE]

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