Osteolysis around the prosthesis and subsequent aseptic loosening are the main causes of prosthesis failure. Inflammation due to wear particles and osteoclast activation are the key factors in osteolysis and are also potential targets for the treatment of osteolysis. However, it is not clear whether puerarin can inhibit chronic inflammation and alleviate osteolysis. In this study, we investigated the effect of puerarin on Ti particle‐induced inflammatory osteolysis in vivo in rat femoral models and in vitro in receptor activator of nuclear factor kappa‐B ligand (RANKL)‐induced osteoclast activation models. Our in vivo results showed that puerarin significantly inhibited Ti particle‐induced osteolysis and the expression of matrix metallopeptidase 9 (MMP‐9), nuclear factor of activated T cells 1 (NFATc1), tumour necrosis factor (TNF)‐α and interleukin (IL)‐6. In vitro, puerarin prevented RANKL‐induced osteoclast differentiation, bone resorption and F‐actin ring formation in a concentration‐dependent manner. Furthermore, puerarin decreased the phosphorylation of p65 and prevented p65 moving from the cytoplasm to the nucleus. Puerarin also reduced the expression of osteoclast‐specific factors and inhibited the inflammatory response. In conclusion, our study proves that puerarin can block the NF‐κB signalling pathway to inhibit osteoclast activation and inflammatory processes, which provides a new direction for the treatment of osteolysis‐related diseases.

中文翻译：

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葛根素通过抑制NF-κB信号通路抑制钛颗粒诱导的骨溶解和RANKL诱导的破骨细胞生成。

假体周围的骨溶解以及随后的无菌性松动是假体失败的主要原因。由于磨损颗粒引起的炎症和破骨细胞活化是溶骨的关键因素，并且也是治疗溶骨的潜在目标。然而，尚不清楚葛根素是否可以抑制慢性炎症并减轻骨溶解。在这项研究中，我们研究了葛根素在大鼠股骨模型中对Ti颗粒诱导的炎症性骨溶解的影响，在体外以及在核因子kappa-B配体（RANKL）诱导的破骨细胞激活模型的受体激活剂中的体外作用。我们的体内结果表明，葛根素能显着抑制Ti颗粒诱导的骨溶解和基质金属肽酶9（MMP-9），活化T细胞1（NFATc1）的核因子的表达，肿瘤坏死因子（TNF）-α和白介素（IL）-6 在体外，葛根素以浓度依赖的方式阻止了RANKL诱导的破骨细胞分化，骨吸收和F-肌动蛋白环的形成。此外，葛根素降低了p65的磷酸化，并阻止了p65从细胞质移至细胞核。葛根素还减少破骨细胞特异性因子的表达并抑制炎症反应。总之，我们的研究证明了葛根素可以阻断NF-κB信号通路，从而抑制破骨细胞的活化和炎症过程，这为治疗与骨溶解相关的疾病提供了新的方向。葛根素降低了p65的磷酸化，并阻止p65从细胞质移至细胞核。葛根素还减少破骨细胞特异性因子的表达并抑制炎症反应。总之，我们的研究证明了葛根素可以阻断NF-κB信号通路，从而抑制破骨细胞的活化和炎症过程，这为治疗与骨溶解相关的疾病提供了新的方向。葛根素降低了p65的磷酸化，并阻止p65从细胞质移至细胞核。葛根素还减少破骨细胞特异性因子的表达并抑制炎症反应。总而言之，我们的研究证明了葛根素可以阻断NF-κB信号通路，从而抑制破骨细胞的活化和炎症过程，为治疗溶骨相关疾病提供了新的方向。