PDF(Pubmed)
Abstract：
Inflammatory reactions are involved in the development of steroid-induced osteonecrosis of the femoral head(ONFH). Studies have explored the therapeutic efficacy of inhibiting inflammatory reactions in steroid-induced ONFH and revealed that inhibiting inflammation may be a new strategy for preventing the development of steroid-induced ONFH. Exosomes derived from M2 macrophages(M2-Exos) display anti-inflammatory properties. This study aimed to examine the preventive effect of M2-Exos on early-stage steroid-induced ONFH and explore the underlying mechanisms involved. In vitro, we explored the effect of M2-Exos on the proliferation and osteogenic differentiation of bone marrow-derived mesenchymal stem cells(BMMSCs). In vivo, we investigated the role of M2-Exos on inflammation, osteoclastogenesis, osteogenesis and angiogenesis in an early-stage rat model of steroid-induced ONFH. We found that M2-Exos promoted the proliferation and osteogenic differentiation of BMMSCs. Additionally, M2-Exos effectively attenuated the osteonecrotic changes, inhibited the expression of proinflammatory mediators, promoted osteogenesis and angiogenesis, reduced osteoclastogenesis, and regulated the polarization of M1/M2 macrophages in steroid-induced ONFH. Taken together, our data suggest that M2-Exos are effective at preventing steroid-induced ONFH. These findings may be helpful for providing a potential strategy to prevent the development of steroid-induced ONFH.
摘要：
炎症反应与激素诱导的股骨头坏死（ONFH）的发展有关。研究已经探索了抑制类固醇诱导的ONFH中的炎症反应的治疗功效，并表明抑制炎症可能是预防类固醇诱导的ONFH发展的新策略。源自M2巨噬细胞的外来体(M2-Exos)显示抗炎特性。本研究旨在研究M2-Exos对早期类固醇诱导的ONFH的预防作用，并探讨其相关机制。体外，我们探讨了M2-Exos对骨髓间充质干细胞（BMMSCs）增殖和成骨分化的影响。在体内,我们研究了M2-Exos对炎症的作用，破骨细胞生成，类固醇诱导的ONFH早期大鼠模型中的成骨和血管生成。我们发现M2-Exos促进BMMSCs的增殖和成骨分化。此外,M2-Exos有效地减弱了骨坏死的变化，抑制促炎介质的表达，促进骨生成和血管生成，减少破骨细胞生成，并调节类固醇诱导的ONFH中M1/M2巨噬细胞的极化。一起来看,我们的数据提示M2-Exos可有效预防类固醇诱导的ONFH.这些发现可能有助于提供预防类固醇诱导的ONFH发展的潜在策略。
