巨噬细胞
巨噬细胞极化
类风湿性关节炎
化学
癌症研究
活性氧
炎症
细胞生物学
关节炎
免疫学
分泌物
细胞凋亡
肿瘤坏死因子α
小干扰RNA
软骨
促炎细胞因子
信号转导
医学
牙周炎
巨噬细胞激活因子
作者
Guogang Zhao,Han Yang,Yating Sun,Xinyi Li,Xiaofang Li,Min Liu,Dan Li,Jiulong Zhang,Xiuli Zhao
出处
期刊:Small
[Wiley]
日期:2025-12-08
卷期号:22 (6): e09576-e09576
被引量:1
标识
DOI:10.1002/smll.202509576
摘要
Rheumatoid arthritis (RA) is an auto-immune disease characterized by inflammatory episodes and joint degradation. Activated macrophages produce large amounts of reactive oxygen species (ROS) and pro-inflammatory cytokines, which damage chondrocytes and destroy the cartilage matrix. Therefore, a promising therapeutic strategy for the treatment of RA is to inhibit the secretion of pro-inflammatory cytokines and ROS to promote macrophage polarization and facilitate cartilage repair. In this paper, an active targeting nanomedicine based on metal-phenolic networks (MPNs) is constructed to re-polarize activated macrophages for RA therapy. Sr2+ and Cu2+ are first coordinated with tannic acid (TA) to prepare TSC, and TNF-α siRNA is loaded into TSC via simple ultrasonic treatment to obtain TSSC. Finally, TSSC is coated with M1 macrophage membrane (termed as TSSC@M1) to enhance its inflammatory targeting ability. TSSC@M1 can actively target macrophages by releasing TA, Cu2+, and TNF-α siRNA to synergistically scavenge ROS and inhibit the expression of TNF-α to induce macrophage polarization, while Sr2+ can further protect cartilage. In the collagen-induced arthritis (CIA) mouse model, TSSC@M1 can accumulate at inflamed joints and alleviate RA symptoms by modulating macrophage phenotype and repairing cartilage. Overall, TSSC@M1 NPs offer a promising and safe approach to treat RA.
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