类固醇诱导的股骨头缺血坏死（SANFH）是一种世界性常见的常见疾病，具有较高的残疾率。过量使用糖皮质激素（GC）是SANFH最常见的非创伤性原因。到目前为止，治疗SANFH的策略有限，并且SANFH进展的机制尚不清楚。然而，骨生成功能障碍被认为是SANFH发展过程中的关键病理生物学机制之一，它涉及小鼠骨髓间质干细胞（BMSC）凋亡和骨生成分化紊乱。熊果酸（UA）是中药方剂右归饮的一个重要成分，具有抗肿瘤、抗炎和骨重塑等广泛的药理特性。由于右归饮对骨重塑有积极作用，本研究旨在研究UA对地塞米松（DEX）诱导的SANFH的体外和体内影响。在体外实验中，我们通过CCK8、Western blotting、TUNEL等方法证实UA可以促进小鼠BMSC增殖并抵抗DEX诱导的细胞凋亡。此外，如ALP和Alizarin红染色实验等体外实验显示，UA对小鼠BMSC的成骨分化具有益处。在体内实验中，H&E染色、免疫组化染色、Elisa和微CT分析结果表明，UA在SANFH模型中具有促进骨修复的作用。此外，Western blot和TUNEL实验的结果显示，UA通过抑制细胞凋亡可以延缓小鼠SANFH的疾病进展。总体而言，我们的研究表明UA是治疗SANFH的潜在化合物。版权所有©2023 Elsevier Inc.发表。

Steroid-induced avascular necrosis of femoral head (SANFH) is a common disorder worldwide with high disability. Overdose of glucocorticoid (GC) is the most common non-traumatic cause of SANFH. Up until now, there are limited therapeutic strategies for curing SANFH, and the mechanisms underlying SANFH progression remain unclear. Nevertheless, Osteogenic dysfunction is considered to be one of the crucial pathobiological mechanisms in the development of SANFH, which involves mouse bone marrow mesenchymal stem cells (BMSCs) apoptosis and osteogenic differentiation disorder. Ursolic acid (UA), an important component of the Chinese medicine formula Yougui Yin, has a wide range of pharmacological properties such as anti-tumor, anti-inflammatory and bone remodeling. Due to the positive effect of Yougui Yin on bone remodeling, the purpose of this study was to investigate the effects of UA on dexamethasone (DEX)-induced SANFH in vitro and vivo. In vitro, we demonstrated that UA can promote mouse BMSCs proliferation and resist DEX-induced apoptosis by CCK8, Western blotting, TUNEL and so on. In addition, vitro experiments such as ALP and Alizarin red staining assay showed that UA had a beneficial effect on the osteogenic differentiation of mouse BMSCs. In vivo, the results of H&E staining, immunohistochemistry staining, Elisa and micro-CT analysis showed that UA had a bone repair-promoting effect in SANFH model. Moreover, the results of Western blot and TUNEL experiments showed that UA could delay the disease progression of SANFH in mice by inhibiting apoptosis. Overall, our study suggests that UA is a potential compound for the treatment of SANFH.Copyright © 2023. Published by Elsevier Inc.