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Edaravone protects osteoblastic cells from dexamethasone through inhibiting oxidative stress and mPTP opening
Wen-xiao Sun1, Hai-ya Zheng2, Jun Lan3
1Department of Orthopedic and Hand Surgery, Liyuan Hospital, Huazhong University of Science and Technology, Wuhan, China.
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.
Insights
Edaravone protects osteoblasts from dexamethasone (Dex)-induced damage by reducing oxidative stress and preventing mitochondrial dysfunction. This study reveals edaravone
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Oxidative stress is implicated in dexamethasone (Dex)-induced osteoblastic cell damage.
- Understanding protective mechanisms against Dex toxicity is crucial for bone health.
Purpose of the Study:
- To investigate the protective effects of edaravone against Dex-induced damage in osteoblastic cells.
- To elucidate the underlying mechanisms of edaravone's action.
Main Methods:
- Assessed cell viability and apoptosis in human and murine osteoblastic cells.
- Measured reactive oxygen species and lipid peroxidation levels.
- Evaluated mitochondrial permeability transition pore (mPTP) opening and membrane potential.
Main Results:
- Edaravone dose-dependently reduced Dex-induced cell death and apoptosis.
- Edaravone inhibited Dex-induced oxidative stress markers (ROS, lipid peroxidation).
- Edaravone repressed Dex-induced mPTP opening, which was essential for its protective effect.
Conclusions:
- Edaravone exhibits significant protective activity against Dex-induced osteoblast damage.
- The mechanism involves the inhibition of oxidative stress and subsequent mPTP opening.
- Edaravone represents a potential therapeutic agent for managing Dex-related bone complications.
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