详细信息
Targeted Ruthenium-Based Anti-Inflammatory Nanoagent for Enhanced Rheumatoid Arthritis Treatment
文献类型:期刊文献
英文题名:Targeted Ruthenium-Based Anti-Inflammatory Nanoagent for Enhanced Rheumatoid Arthritis Treatment
作者:Zhao, Ziwei[1];Xiong, Hao[2];Wu, Jinyong[1];Xu, Shiyu[1];Zhao, Lihua[1];Wang, Yanshuai[1];Chen, Shuai[2];Fan, Cunyi[2];Niu, Dechao[1]
机构:[1]East China Univ Sci & Technol, Frontier Sci Ctr Mat Biol & Dynam Chem, Sch Mat Sci & Engn, Key Lab Ultrafine Mat Minist Educ, Shanghai, Peoples R China;[2]Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 6, Sch Med, Dept Orthoped, Shanghai, Peoples R China
年份:2025
卷号:5
期号:5
外文期刊名:EXPLORATION
收录:WOS:【ESCI(收录号:WOS:001550458900001)】;
基金:This work was financially supported by the National Natural Science Foundation of China (Grant Number: 52072124 and 32371406), the Program of Shanghai Academic/Technology Research Leader (Grant Number: 22XD1421100), the Fundamental Research Funds for the Central Universities, and the 111 project (Grant Number: B14018).
语种:英文
外文关键词:anti-inflammatory; organosilica; photothermal; rheumatoid arthritis; ruthenium
摘要:The inhibition of joint synovial inflammation, caused by poor oxygen (O2) supply and excessive reactive oxygen species (ROS) generation, is an important treatment strategy for rheumatoid arthritis (RA). Herein, we formulated a targeted ruthenium-based anti-inflammatory nanosystem consisting of ruthenium clusters-loaded F127-organosilica micelles with folic acid (FA) modification (RuFOMs-FA) for RA treatment through a two-stage macrophage regulatory mechanism. At the first stage, RuFOMs-FA exhibited excellent photothermal capability with a high photothermal conversion efficiency of 55.3% upon external-field 808 nm NIR irradiation, which further induced the death of M1 macrophages through the folic acid-mediated active targeting pathway. Further, the resultant nanoagent mimicked enzymes displayed catalase-like and superoxide dismutase-like activities for endogenously scavenging ROS and producing O2 to induce the polarization of pro-inflammatory M1 to anti-inflammatory M2 macrophages in the RA physiological environment. More importantly, RuFOMs-FA effectively alleviated hypoxia, inflammation, and cartilage destruction in the synovial joints in a rat RA model by the two-stage macrophage regulatory mechanism. Consequently, it is highly expected that the developed RuFOMs-FA could be applied as a new noble metal-based anti-inflammatory candidate nanosystem for efficient and safe RA treatment.
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