脂联素通过抑制 NF-κB 和 p38 信号通路抑制破骨细胞分化。
Adiponectin inhibits osteoclastogenesis by suppressing NF-κB and p38 signaling pathways.
机构信息
Department of Orthopedics, The First Affiliated Hospital of Nanchang University, Artificial Joints Engineering and Technology Research Center of Jiangxi Province, Nanchang, Jiangxi province, 330006, China; Multidisciplinary Therapy Center of Musculoskeletal Tumor, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi province, 330006, China.
Department of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi province, 330006, China.
出版信息
Biochem Biophys Res Commun. 2018 Sep 10;503(3):2075-2082. doi: 10.1016/j.bbrc.2018.07.162. Epub 2018 Aug 11.
Adiponectin (APN) has been shown to play a key role in regulating bone mineral density (BMD). Nevertheless, the effects of APN on receptor activator of NF-κB ligand (RANKL)-induced osteoclast formation and mechanism of regulation are not entirely clear. The study, therefore, aimed to evaluate the effect of APN on osteoclastogenesis. Our results showed that APN inhibits osteoclastogenesis and resorption function in vitro by suppressing nuclear factor-κB (NF-κB) and p38 signaling pathways, which is essential for osteoclast formation. Moreover, APN blocked the formation of F-actin rings and attenuated osteoclast-mediated bone resorptive function. Therefore, we concluded that APN may provide a potential treatment for osteoclast-related diseases, such as osteoporosis.
脂联素 (APN) 已被证明在调节骨密度 (BMD) 方面发挥着关键作用。然而，APN 对核因子-κB 配体 (RANKL) 诱导的破骨细胞形成的影响及其调节机制尚不完全清楚。因此，本研究旨在评估 APN 对破骨细胞生成的影响。我们的结果表明，APN 通过抑制核因子-κB (NF-κB) 和 p38 信号通路来抑制体外破骨细胞的生成和吸收功能，这对破骨细胞的形成至关重要。此外，APN 阻断 F-肌动蛋白环的形成并减弱破骨细胞介导的骨吸收功能。因此，我们得出结论，APN 可能为破骨细胞相关疾病（如骨质疏松症）提供一种潜在的治疗方法。
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