Abstract
PurposeGlucocorticoid-induced osteonecrosis of the femoral head (GIONFH) is a common disease following long-term use or large doses of glucocorticoids. The pathogenesis of GIONFH remains controversial, and abnormal bone metabolism caused by glucocorticoids(GCs) may be one of the important factors. Due to its positive effect on bone remodeling, naringin shows potential therapeutic effects in bone metabolism-related diseases. In this study, we hypothesized that naringin regulated bone metabolism in rat GIONFH via the Akt/Bad signal cascades. MethodsIn vitro, a dexamethasone (Dex)- or naringin-treated cell model was used to evaluate the function of naringin. In vivo, methylprednisolone (MPS)-treated rat model was used to evaluate the function of naringin in GIONFH. In vitro, Cell Counting Kit-8 (CCK-8) and Edu staining was used to evaluate the proliferation of osteocytes, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, Annexin V-FITC-PI, and western blotting were used to evaluate the apoptosis of osteocytes. We also verified the effects of naringin on osteogenesis and osteoclastogenesis. In vivo, we used micro-CT (computed tomography), histological, and immunohistochemical analysis to evaluate the effect of naringin. Moreover, the mechanism of naringin regulating the bone metabolism through the Akt/Bad pathway was also investigated using bioinformatics analysis and western blotting. ResultsThe results of in vitro study showed that Akt activated by naringin promoted osteogenesis and osteocyte proliferation; in addition, osteocyte apoptosis and osteoclastogenesis was inhibited by Akt activation and Bad suppression. According to the in vivo study, naringin prevented GIONFH in a rat model as shown by micro-CT scanning and histological and immunohistochemical analysis. ConclusionsTherefore, we concluded that naringin is an effective compound for promoting bone repair and preventing bone loss in rats with GIONFH through Akt/Bad signal cascades.
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