Department of Sports Medicine, Qilu Hospital (Qingdao), Cheeloo College of Medicine, Shandong University, Qingdao, Shandong 266035, China.
Department of Orthopaedics, Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China.
Cell Mol Biol (Noisy-le-grand). 2023 May 31;69(5):94-104. doi: 10.14715/cmb/2023.69.5.16.
The excessive steroid may cause dyslipidaemia and oxidative insult during femoral head osteonecrosis, inducing bone loss and impairment of the intraosseous blood system. In contrast, bio-flavanone naringin has shown antioxidant, antiresorptive and lipid-lowering bioactivities. The present research is an effort to explore the anti-ON potential of naringin in vivo and in vitro. After a 6-week treatment, the femora were dissected for histological examination following bone mineral density assay by X-ray absorptiometry. Blood samples were examined for coagulation, oxidative stress, lipid transportation and endothelial injury. Marrow samples were cultured and assayed for adipogenic and osteogenic alterations by ALP activity, mineralization, RT-qPCR and western blot analysis. The results showed that naringin exerted a dose-dependent effect on reducing ON incidence, with inhibition of osteoporosis, oxidative stress and dyslipidaemia. The mechanism included the suppression of PPARγ2 for adipogenesis of bone marrow stem cells (BMSCs) and the prevention of oxidative stress in endothelium injury. Naringin may restore steroid-impaired osteogenesis by enhancing the mRNA and protein expression of osteogenic markers in a dose-ascending manner and new bone formation can be found in naringin groups. Taken together, our findings showed that naringin may serve as a prophylactic agent and selective PPARγ modulator for the early-stage ON.
过量的类固醇可能会导致股骨头坏死过程中的血脂异常和氧化损伤，从而导致骨质流失和骨内血供系统受损。相比之下，类黄酮柚皮苷具有抗氧化、抗吸收和降血脂的生物活性。本研究旨在探索柚皮苷在体内和体外的防治骨坏死的潜力。经过 6 周的治疗后，通过 X 射线吸收法测定骨密度，对股骨进行组织学检查和解剖。检查血液样本的凝血、氧化应激、脂质转运和内皮损伤情况。骨髓样本进行培养，并通过碱性磷酸酶（ALP）活性、矿化、RT-qPCR 和 Western blot 分析检测成脂和成骨的变化。结果表明，柚皮苷对降低骨坏死的发生率具有剂量依赖性，可抑制骨质疏松、氧化应激和血脂异常。其作用机制包括抑制骨髓间充质干细胞（BMSCs）的过氧化物酶体增殖物激活受体γ 2（PPARγ2）的成脂分化，预防内皮细胞氧化应激损伤。柚皮苷可通过增强成骨标志物的 mRNA 和蛋白表达，以剂量递增的方式恢复类固醇引起的成骨作用，并可在柚皮苷组中发现新骨形成。综上所述，我们的研究结果表明，柚皮苷可能作为一种预防剂和选择性过氧化物酶体增殖物激活受体γ（PPARγ）调节剂，用于早期骨坏死。
