In recent times, there has been growing attention towards exploring the nutritional and functional aspects of potato protein, along with its diverse applications. In the present study, we examined the anti‐osteoclast properties of potato protein hydrolysate (PP902) in vitro. Murine macrophages (RAW264.7) were differentiated into osteoclasts by receptor activator of nuclear factor‐κB ligand (RANKL), and PP902 was examined for its inhibitory effect. Initially, treatment with PP902 was found to significantly prevent RANKL‐induced morphological changes in macrophage cells, as determined by tartrate‐resistant acid phosphatase (TRAP) staining analysis. This notion was further supported by F‐actin analysis using a confocal microscope. Furthermore, PP902 treatment effectively and dose‐dependently down‐regulated the expression of RANKL‐induced osteoclastogenic marker genes, including TRAP, CTR, RANK, NFATc1, OC‐STAMP, and c‐Fos. These inhibitory effects were associated with suppressing NF‐κB transcriptional activation and subsequent reduced nuclear translocation. The decrease in NF‐κB activity resulted from reduced activation of its upstream kinases, including I‐κBα and IKKα. Moreover, PP902 significantly inhibited RANKL‐induced p38MAPK and ERK1/2 activities. Nevertheless, PP902 treatment prevents RANKL‐induced intracellular reactive oxygen species generation via increased HO‐1 activity. The combined antioxidant and anti‐inflammatory effects of PP902 resulted in significant suppression of osteoclastogenesis, suggesting its potential as an adjuvant therapy for osteoclast‐related diseases.

中文翻译：

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马铃薯蛋白水解物通过 NF-κB/MAPKs 信号通路抑制破骨细胞生成基因，从而抑制 RANKL 诱导的破骨细胞发育

近年来，人们越来越关注探索马铃薯蛋白质的营养和功能方面及其多样化应用。在本研究中，我们在体外检测了马铃薯蛋白水解物（PP902）的抗破骨细胞特性。小鼠巨噬细胞（RAW264.7）通过核因子κB配体受体激活剂（RANKL）分化为破骨细胞，并检查PP902的抑制作用。最初，通过抗酒石酸酸性磷酸酶 (TRAP) 染色分析确定，PP902 治疗可显着预防 RANKL 诱导的巨噬细胞形态变化。使用共焦显微镜进行的 F-肌动蛋白分析进一步支持了这一观点。此外，PP902 治疗有效且剂量依赖性地下调 RANKL 诱导的破骨细胞标记基因的表达，包括陷阱,点击率,秩,NFATc1,OC-STAMP， 和c-Fos。这些抑制作用与抑制 NF-κB 转录激活和随后减少的核转位有关。 NF-κB 活性的降低是由于其上游激酶（包括 I-κBα 和 IKKα）的激活减少所致。此外，PP902 显着抑制 RANKL 诱导的 p38MAPK 和 ERK1/2 活性。尽管如此，PP902 治疗可通过增加 HO-1 活性来防止 RANKL 诱导的细胞内活性氧的产生。 PP902 的抗氧化和抗炎作用可显着抑制破骨细胞生成，表明其作为破骨细胞相关疾病的辅助治疗的潜力。