【摘要】 过量激素刺激骨髓间质干细胞(bone marrow stromal cells, BMSCs)使得成骨能力减弱、成脂能力增强是导致股骨头坏死(osteonecrosis of the femoral head, ONFH)的主要原因,调控机制尚未阐明。最新的研究发现激素引起骨组织中11β-HSD1活性增强,导致骨局部内源性激素积聚可抑制骨形成。抑制11β-HSD1活性可促进成骨细胞分化,抑制脂肪分化。故推测内源性激素在ONFH的发病过程中起到重要作用,在激素与BMSCs活性变化之间可能存在11β-HSD1调控的内源性激素代谢途径参与ONFH的发病过程。因此,深入研究11β-HSD1介导的内源性激素代谢途径在ONFH发病中的作用,对深入了解ONFH的发病机制具有重要意义。更多还原

【Abstract】 One of the main causes of steroid-induced osteonecrosis of the femoral head(SIONFH) is resulted from low osteogenesis and high adipogenesis of bone marrow mesenchymal stem cells(BMSCs) stimulated by excess glucocorticoid-used,nevertheless the mechanisms are not understood completely. Some studies have found that glucocorticoid induced the increase of 11 beta-hydroxysteroid dehydrogenase 1(11β-HSD1) activity in bone tissue, leaded to endogenous glucocorticoid accumulation and inhibited bone formation. Inhibition of 11β-HSD1 activity did promote osteoblasts differentiation, inhibit fat differentiation and formation of atherosclerotic plaque in mice. It is speculated that there is glucocorticoid metabolism in bone tissue regu-lated by 11β-HSD1 in patients with SIONFH, and there may be an endogenous hormone metabolic pathway regulated by 11β-HSD1 in the process of the pathogenesis of SIONFH between the changes of hormone and BMSCs activity. Therefore, researching the roles of 11β-HSD1-mediated endogenous hormone metabolic pathway in SIONFH might help us further understand the pathogenesis of SIONFH.更多还原