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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.

Author information

1
Department of Orthopedic and Hand Surgery, Liyuan Hospital, Huazhong University of Science and Technology, Wuhan, China.
2
Department of Clinical Laboratory, The People's Hospital of Lishui, Lishui, 323000, Zhejiang, China.
3
Department of Orthopaedics, The People's Hospital of Lishui, Lishui, 323000, Zhejiang, China. clinlablanjunls@163.com.

Abstract

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.

KEYWORDS:

Dexamethasone; Edaravone; Osteoblasts; Osteonecrosis; Oxidative stress

PMID:
26179849
DOI:
10.1007/s11010-015-2511-2
[Indexed for MEDLINE]

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