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

机译:地塞米松促进间充质干细胞凋亡,通过破坏线粒体动力学来抑制骨肉发生

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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 (10sup?6/sup?mol·Lsup?1/sup) decreased cell activity, promoted apoptosis, elevated levels of reactive oxygen species and disrupted mitochondrial dynamics. Furthermore, dexamethasone (10sup?6/sup?mol·Lsup?1/sup) inhibited osteogenesis of stem cells and promoted adipogenesis. These findings may facilitate greater understanding of the adverse effects of dexamethasone on the femoral head.
机译:长期或大量使用糖皮质激素会导致股骨头的严重坏死,但潜在的机制仍然不清楚。最近的研究发现,线粒体动力学在股骨头坏死中发挥着重要作用。在这里,我们研究了地塞米松对间充质干细胞线粒体功能的影响。我们观察到,高浓度的地塞米松(10 β6?mol·Lβ1)降低细胞活性,促进细胞凋亡,活性氧物种的升高,并破坏线粒体动力学。此外,地塞米松(10 β6?mol·Lβ1)抑制干细胞的骨质发生并促进脂肪发生。这些发现可以促进对地塞米松对股骨头的不良反应的了解。

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