Apocynin exerts cytoprotective effects on dexamethasone‐induced osteoblasts by inhibiting oxidative stress through the Nrf2 signalling pathway

Author:

Zhang Xinglong1ORCID,Pang Ran1,Zhang Kai2,Xu Qian3,Xu Chunlei2,Shi Wei2,Liang Xinyu2,Li Dong2,Cui Wenhao45,Bai Shucai6,Li Zhijun2,Li Hui1,Zhang Huafeng2

Affiliation:

1. Department of Orthopaedics TianjinNankai Hospital Tianjin China

2. Department of Orthopaedics General Hospital of Tianjin Medical University Tianjin China

3. School of Integrative Medicine Tianjin University of Traditional Chinese Medicine Tianjin China

4. Department of Pharmacology Kyoto Prefectural University of Medicine Kyoto Japan

5. R&D Center Youjia (Hangzhou) Biomedical Technology Co., Ltd Hangzhou China

6. Department of Orthopaedics Tianjin Hospital Tianjin China

Abstract

AbstractSteroid‐induced femoral head necrosis (SIFHN) is a serious clinical complication that is caused by prolonged or excessive use of glucocorticoids (GCs). Osteoblast apoptosis and osteogenic differentiation dysfunction caused by GC‐induced oxidative stress and mitochondrial impairment are strongly implicated in SIFHN. Apocynin (APO) is a kind of acetophenone extracted from an herb. In recent years, APO has received much attention for its antiapoptotic and antioxidant properties. This study aimed to investigate whether APO could protect against SIFHN and explore the mechanism. In our study, low‐dose APO had no toxic effects on osteoblasts and restored dexamethasone (Dex)‐treated osteoblasts by improving survival, inhibiting OS and restoring mitochondrial dysfunction. Mechanistically, APO alleviated Dex‐induced osteoblast injury by activating the Nrf2 pathway, and the use of ML385 to block Nrf2 significantly eliminated the protective effect of APO. In addition, APO could reduce the formation of empty lacunae, restore bone mass and promote the expression of Nrf2 in SIFHN rats. In conclusion, APO protects osteoblasts from Dex‐induced oxidative stress and mitochondrial dysfunction through activation of the Nrf2 pathway and may be a beneficial drug for the treatment of SIFHN.

Publisher

Wiley

Subject

Cell Biology,Molecular Medicine

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