破骨细胞
氧化应激
硒蛋白
骨溶解
活性氧
硒
GPX1型
兰克尔
硒代半胱氨酸
癌症研究
化学
细胞生物学
激活剂(遗传学)
生物化学
生物
医学
谷胱甘肽过氧化物酶
体外
超氧化物歧化酶
酶
半胱氨酸
外科
有机化学
基因
作者
Binhua Zou,Zushuang Xiong,Yanzi Yu,Sujiang Shi,Xiaoling Li,Tianfeng Chen
标识
DOI:10.1002/adma.202401620
摘要
Abstract Osteoclast hyperactivation stands as a significant pathological factor contributing to the emergence of bone disorders driven by heightened oxidative stress levels. The modulation of the redox balance to scavenge reactive oxygen species (ROS) emerges as a viable approach in addressing this concern. Selenoproteins, characterized by selenocysteine (SeCys 2 ) as the active center, are crucial for selenium‐based antioxidative stress therapy for inflammatory diseases. This study reveals that surface‐active elemental selenium (Se) nanoparticles, particularly those derived from lentinan (LNT‐Se), exhibit enhanced cellular accumulation and accelerated metabolism to SeCys 2 , the primary active Se form in biological systems. Consequently, LNT‐Se demonstrates significant inhibition of RANKL‐induced osteoclastogenesis and osteoclastic activity when compared to alternative Se species. Furthermore, in vivo studies underscore the superior therapeutic efficacy of LNT‐Se over SeCys 2 , potentially attributable to the enhanced stability and safety profile of LNT‐Se. Specifically, LNT‐Se effectively modulates the expression of the selenoprotein GPx1, thereby exerting regulatory control over macrophage polarization, osteoclast activity inhibition, and the prevention of CIA/OVX‐induced osteolysis. In summary, these results suggest that the prompt activation of selenoproteins by Se nanoparticles serves to suppress osteoclastogenesis and pathological bone loss by upregulating GPx1 to re‐polarize macrophages. Moreover, the utilization of bioactive Se species presents a promising avenue for effectively managing bone disorders, with considerable potential for clinical translation. This article is protected by copyright. All rights reserved
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