巨噬细胞极化
化学
软骨细胞
骨关节炎
串扰
癌症研究
车站3
蓝蛋白
白桦酸
细胞生物学
趋化因子
炎症
流式细胞术
药理学
关节炎
受体
M2巨噬细胞
激酶
生物化学
甘露糖受体
白藜芦醇
滑膜炎
荧光各向异性
免疫系统
细胞毒性
软骨
作者
Qin‐Wen Liu,Yupeng Chen,Xiaoyan Zhuang,Jingxin Liu,Haojie Chen,Zhenyi Shi,Xiang Li,Yiwen Li,Qian Luo,Hangtian Wu,Yanpeng Lin,Wanling He,Runjie Yu,Yi Li,Xiaohong Gong,Maolin Wang,Jun Wang,Jianjun Chen,Aiping Lü,Cheng Zhou
出处
期刊:Small
[Wiley]
日期:2025-10-28
卷期号:21 (50): e09306-e09306
被引量:2
标识
DOI:10.1002/smll.202509306
摘要
Osteoarthritis (OA) is a degenerative joint disease characterized by M1 macrophage-driven synovitis, worsening progression. In this study, it is found that betulinic acid (BA), a natural compound, inhibits M1 macrophage characteristics while promoting conversion to the M2 phenotype. However, BA suffers from poor solubility and a short half-life in vivo, restricting therapeutic use. Here, a thermosensitive hydrogel is developed using hydroxypropyl chitosan, loaded with poly(betulinic acid) nanoparticles (PBA NPs) and a folic acid (FA) targeting moiety, yielding FA-modified PBA NPs-loaded hydrogel (FA-PBA NPs@Gel) with sustained release, injectability, and enhanced stability. FA-PBA NPs@Gel selectively targets M1 macrophages via FA-folate receptor 1 interaction to alleviate synovitis, while disrupting macrophage-chondrocyte crosstalk to foster cartilage regeneration. Immunofluorescence and flow cytometry demonstrate reprogramming of M1 to M2. Transcriptome sequencing, antibody microarrays, and drug affinity responsive target stability assays show that FA-PBA NPs@Gel suppressed nuclear factor-κB (NF-κB) activation by binding glycogen synthase kinase 3 beta (GSK3β), thereby downregulating chemokine ligand 20 (CCL20), disrupting macrophage-chondrocyte crosstalk and promoting cartilage regeneration. In summary, FA-PBA NPs@Gel represent a promising OA therapy with dual functions of mitigating synovitis and promoting regeneration.
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