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金纳米颗粒通过作为抗氧化剂抑制核因子-κB受体激活剂配体（RANKL）诱导的破骨细胞形成。

Gold nanoparticles inhibited the receptor activator of nuclear factor-κb ligand (RANKL)-induced osteoclast formation by acting as an antioxidant.

作者信息

Sul Ok-Joo, Kim Jin-Chun, Kyung Tae-Wook, Kim Hye-Jin, Kim Youn-Young, Kim Song-Hee, Kim Ji-Soon, Choi Hye-Seon

机构信息

Department of Biological Sciences (BK21 Program) and Immunomodulation Research Center, University of Ulsan, Korea.

出版信息

Biosci Biotechnol Biochem. 2010;74(11):2209-13. doi: 10.1271/bbb.100375. Epub 2010 Nov 7.

DOI:10.1271/bbb.100375
PMID:21071867
Abstract

Gold nanoparticles inhibited osteoclast (OC) formation induced by the receptor activator of nuclear factor-κB ligand (RANKL) in bone marrow-derived macrophages (BMMs). This was accompanied by a decreased level of tartrate-resistant alkaline phosphatase (TRAP) and less activation of nuclear factor (NF)-κB. The nanoparticles also reduced the production of reactive oxygen species (ROS) in response to RANKL and upregulated RANKL-induced glutathione peroxidase-1 (Gpx-1), suggesting a role as an antioxidant in the BMM. The inhibitory effects on OC formation might have been due to elevated defense against oxidative stress.

摘要

金纳米颗粒抑制了骨髓来源巨噬细胞（BMMs）中由核因子-κB配体（RANKL）诱导的破骨细胞（OC）形成。这伴随着抗酒石酸酸性磷酸酶（TRAP）水平的降低以及核因子（NF）-κB的激活减少。纳米颗粒还降低了对RANKL反应时活性氧（ROS）的产生，并上调了RANKL诱导的谷胱甘肽过氧化物酶-1（Gpx-1），表明其在BMMs中具有抗氧化作用。对OC形成的抑制作用可能归因于对氧化应激的防御增强。

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