Dexamethasone promotes mesenchymal stem cell apoptosis and inhibits osteogenesis by disrupting mitochondrial dynamics

被引:25
|
作者
Ma, Liang [1 ]
Feng, Xiaobo [1 ]
Wang, Kun [1 ]
Song, Yu [1 ]
Luo, Rongjin [1 ]
Yang, Cao [1 ]
机构
[1] Huazhong Univ Sci & Technol, Union Hosp, Dept Orthoped, Tongji Med Coll, Wuhan 430022, Hubei, Peoples R China
来源
FEBS OPEN BIO | 2020年 / 10卷 / 02期
基金
国家重点研发计划; 中国国家自然科学基金;
关键词
apoptosis; dexamethasone; mesenchymal stem cells; mitochondria; osteogenesis; salvianolic acid B; SALVIANOLIC-ACID-B; UP-REGULATION; STRESS; SIRT3; DIFFERENTIATION; MILTIORRHIZAE; RADIX;
D O I
10.1002/2211-5463.12771
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Long-term or heavy use of glucocorticoids can cause severe necrosis of the femoral head, but the underlying mechanisms are still unclear. Recent studies have found that mitochondrial dynamics play an important role in femoral head necrosis. Here, we investigated the effect of dexamethasone on the mitochondrial function of mesenchymal stem cells. We observed that high concentrations of dexamethasone (10(-6) mol center dot L-1) decreased cell activity, promoted apoptosis, elevated levels of reactive oxygen species and disrupted mitochondrial dynamics. Furthermore, dexamethasone (10(-6) mol center dot L-1) inhibited osteogenesis of stem cells and promoted adipogenesis. These findings may facilitate greater understanding of the adverse effects of dexamethasone on the femoral head.
引用
收藏
页码:211 / 220
页数:10
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