Yuan Na, Li Jia, Li Meng, Ji Wenchen, Ge Zhaogang, Fan Lihong, Wang Kunzheng
Department of Ultrasonography, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, People's Republic of China.
Department of Orthopedics, The First Affiliated Hospital of Xi'an Jiaotong University, 277 West Yanta Road, Xi'an, Shaanxi, 710061, People's Republic of China.
BMC Musculoskelet Disord. 2018 Apr 27;19(1):129. doi: 10.1186/s12891-018-2050-6.
It was indicated that inhibition of PPARγ probably represents a novel therapy for steroid-related osteonecrosis. In this study, we investigated the preventive effects of PPARγ inhibition on steroid-related osteonecrosis in a rabbit model.
Rabbits were randomly divided into three groups (normal group, model group and BADGE group). Osteonecrosis was induced in rabbits in the model group and the BADGE group. The BADGE group also received bisphenol a diglycidyl ether(BADGE), a PPARγ antagonist, for 6 weeks.
Histopathological results indicated that rabbits treated with BADGE exhibited significantly reduced osteonecrotic changes, incidence of osteonecrosis and bone marrow adiposity. Furthermore, BADGE-treated rabbits exhibited reduced intraosseous pressure and increased femoral blood perfusion. Micro-computed tomography and bone histomorphometry indicated that the BADGE group exhibited significantly improved bone quality and mineral appositional rate compared with the model group. Furthermore, the BADGE group showed a significant increase in circulating levels of the bone formation marker osteocalcin and reduced levels of the bone resorption marker TRACP. Overall, BADGE-treated rabbits exhibited reduced marrow adiposity concomitant with improved bone formation.
In conclusion, these observations demonstrated that pharmacological inhibition of PPARγ might represent an effective therapy for steroid-related osteonecrosis in the near future.
有研究表明，抑制过氧化物酶体增殖物激活受体γ（PPARγ）可能是一种治疗类固醇相关骨坏死的新方法。在本研究中，我们在兔模型中研究了抑制PPARγ对类固醇相关骨坏死的预防作用。
将兔子随机分为三组（正常组、模型组和BADGE组）。对模型组和BADGE组的兔子诱导骨坏死。BADGE组还接受了PPARγ拮抗剂双酚A二缩水甘油醚（BADGE）治疗6周。
组织病理学结果表明，接受BADGE治疗的兔子骨坏死变化、骨坏死发生率和骨髓脂肪变性显著降低。此外，接受BADGE治疗的兔子骨内压压压力降低，股骨血液灌注增加。显微计算机断层扫描和骨组织形态计量学表明，与模型组相比，BADGE组的骨质量和矿物质沉积率显著改善。此外，BADGE组骨形成标志物骨钙素的循环水平显著升高，骨吸收标志物抗酒石酸酸性磷酸酶（TRACP）水平降低。总体而言，接受BADGE治疗的兔子骨髓脂肪变性减少，同时骨形成得到改善。
总之，这些观察结果表明，PPARγ的药物抑制在不久的将来可能是治疗类固醇相关骨坏死的有效方法。
