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瑞香素通过AMPK/mTOR通路减轻痛风性关节炎的炎症并促进自噬。

Daphnetin alleviates inflammation and promotes autophagy via the AMPK/mTOR pathway in gouty arthritis.

作者信息

Liu Zhiyong, Chu Aichun, Bai Zhiqian, Yang Chao

机构信息

Department of Rheumatology and Immunology Renmin Hospital Wuhan University Wuhan Hubei China.

Department of Orthopedics Maternal and Child Health Hospital of Hubei Province Wuhan China.

出版信息

J Cell Commun Signal. 2025 Apr 28;19(2):e70011. doi: 10.1002/ccs3.70011. eCollection 2025 Jun.

Abstract

Gouty arthritis (GA) is an inflammatory disease resulting from monosodium urate (MSU) crystal deposition in joints and surrounding tissues. Daphnetin (DAP) is a coumarin derivative with potent anti-inflammatory activity. Nonetheless, whether DAP can protect against MSU-induced acute GA remains unclarified. In this study, C57BL/6 mice were injected intra-articularly with MSU crystal suspension to induce acute GA. THP-1 cells were stimulated with MSU to mimic the microenvironment of GA in vitro. Hematoxylin-eosin staining was conducted to observe the pathological changes in mouse synovial tissues. ELISA and RT-qPCR were employed for inflammatory cytokine level determination. Immunofluorescence staining was performed to estimate LC3 expression in THP-1 cells. Western blotting was used for protein expression analysis. The results showed that DAP pretreatment mitigated MSU-elicited ankle joint swelling and synovial damage in mice. Moreover, DAP hindered proinflammatory factor expression and promoted autophagy in MSU-stimulated GA mice and THP-1 cells. Mechanistically, DAP induced AMPK activation and mTOR inactivation. Blocking AMPK signaling counteracted DAP-mediated effects on inflammation and autophagy in MSU-stimulated THP-1 cells. In conclusion, DAP prevents MSU-elicited GA by alleviating inflammation and enhancing autophagy via AMPK/mTOR signaling transduction.

摘要

痛风性关节炎(GA)是一种由于单钠尿酸盐(MSU)晶体沉积在关节及周围组织而导致的炎症性疾病。瑞香素(DAP)是一种具有强大抗炎活性的香豆素衍生物。然而,DAP是否能预防MSU诱导的急性GA仍不明确。在本研究中,向C57BL/6小鼠关节腔内注射MSU晶体悬液以诱导急性GA。用MSU刺激THP-1细胞以在体外模拟GA的微环境。进行苏木精-伊红染色以观察小鼠滑膜组织的病理变化。采用ELISA和RT-qPCR测定炎症细胞因子水平。进行免疫荧光染色以评估THP-1细胞中LC3的表达。使用蛋白质印迹法进行蛋白质表达分析。结果表明,DAP预处理减轻了MSU引起的小鼠踝关节肿胀和滑膜损伤。此外,DAP抑制了MSU刺激的GA小鼠和THP-1细胞中促炎因子的表达并促进了自噬。机制上,DAP诱导AMPK激活和mTOR失活。阻断AMPK信号可抵消DAP对MSU刺激的THP-1细胞中炎症和自噬的介导作用。总之,DAP通过AMPK/mTOR信号转导减轻炎症并增强自噬来预防MSU诱导的GA。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9a9/12037417/5a293f8b4c39/CCS3-19-e70011-g001.jpg

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