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Naringin nanoparticles alleviate RA-ILD pulmonary fibrosis by targeting 14-3-3ζ to inhibit LYVE1+macrophages TGF-β1 secretion 期刊论文

编号：

8AE6BFD83787623AE021135254EBEA4E
作者：

Li, Xiaohan#^[1,2,8]Wang, Jianzhu^[3,4];Zhang, Xiaoyu^[5];Wang, Xilong^[1,2];Sun, Chengxi(孙成玺)^[1,2]Zhao, Na(赵娜)^[1,2]Liu, Zhipu^[1,2];Schioth, Helgi B.^[6];Wang, Hongxing(王洪星)*^[1,2,7]Zhang, Yi(张义)*^[1,2,7]
语种：

英文
期刊：

MATERIALS TODAY BIO ISSN：2590-0064 2026 年 37 卷 ; APR
收录：
关键词：

Naringin nanoparticles RA-ILD LYVE1+macrophages 14-3-3 zeta TGF-beta 1 Flavonoid
摘要：

Background: Rheumatoid arthritis (RA)-interstitial lung disease (RA-ILD) is an idiopathic complication of RA that presents as pulmonary fibrosis. Despite extensive research, the exact cause of RA-ILD remains elusive, driving the ongoing search for effective treatments. Methods: Transcriptomes of lung tissues from both healthy individuals and patients with RA-ILD were analyzed to identify differentially expressed genes. CMAP identified the flavonoid naringin (NAR) as a potential drug for RA-ILD treatment. Subsequently, NAR nanoparticles were developed and orally administered to a collagen-induced arthritis ILD (CIA-ILD) model in DBA/1 mice. Transcriptome and protein profiling analyses using microscale thermophoresis and cellular thermal shift analysis were conducted to predict and confirm the downstream molecules and targets of NAR therapy in RA-ILD. Additionally, an in vitro pulmonary fibrosis model was established to investigate the specific mechanism of NAR treatment in CIA-ILD. Results: In animal experiments, treatment with NAR nanoparticles significantly reduced pulmonary fibrosis in CIA-ILD mice compared with untreated mice. Moreover, there was a notable increase in the number of lymphatic vessel endothelial receptor-1 positive (LYVE1+) macrophages in the lung tissue. Mechanistically, NAR increased LYVE1 levels in macrophages by targeting 14-3-3 zeta. In vitro experiments demonstrated that NAR-treated LYVE1+ bronchoalveolar macrophages (LYVE1+ BLM) effectively inhibited epithelial-mesenchymal transition of A549 cells and fibroblast-myofibroblast transition of HFL1 cells by reducing the secretion of transforming growth factor beta-1. Conclusion: Our research revealed NAR as a novel reference drug for treating RA-ILD, while also identifying potential therapeutic target cells and avenues for drug development in this context. Further comprehensive research is warranted to extend these findings and benefit a broader population of patients with RA-ILD pulmonary fibrosis.
推荐引用方式
GB/T 7714：

Li Xiaohan,Wang Jianzhu,Zhang Xiaoyu, et al. Naringin nanoparticles alleviate RA-ILD pulmonary fibrosis by targeting 14-3-3ζ to inhibit LYVE1+macrophages TGF-β1 secretion [J].MATERIALS TODAY BIO,2026,37.
APA：

Li Xiaohan,Wang Jianzhu,Zhang Xiaoyu,Wang Xilong,&Zhang Yi.(2026).Naringin nanoparticles alleviate RA-ILD pulmonary fibrosis by targeting 14-3-3ζ to inhibit LYVE1+macrophages TGF-β1 secretion .MATERIALS TODAY BIO,37.
MLA：

Li Xiaohan, et al. "Naringin nanoparticles alleviate RA-ILD pulmonary fibrosis by targeting 14-3-3ζ to inhibit LYVE1+macrophages TGF-β1 secretion" .MATERIALS TODAY BIO 37(2026).
入库时间：

4/1/2026 10:03:19 PM
更新时间：

4/1/2026 10:03:19 PM

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