ArticleJournal of inflammation research2025
Calycosin-7-Glucoside Alleviates Atherosclerosis by Inhibiting Ox-LDL-Induced Foam Cell Formation and Inflammatory Response in THP-1-Derived Macrophages via ATF-1 Activation Through the p38/MAPK Pathway.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- STAT2-IRF1-ISG15-Associated Temporal Immune Reprogramming in Macrophages during Aspergillus fumigatus Infection.Current microbiology · 2026Article
- Integrating Network Pharmacology and In Vitro Experiments to Elucidate the Antiatherosclerotic Mechanisms of Qingxin Tongmai Yin.Mediators of inflammation · 2026Article
- Calycosin ameliorates inflammation and M1 macrophage polarization via Spon2 in LPS-triggered MH-S alveolar macrophages.Journal of natural medicines · 2025Article
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Authors and funding
6 authors.
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Abstract
Purpose: Macrophages play a pivotal role in the progression of atherosclerosis (AS), and targeting macrophage-associated pathological processes has emerged as a promising therapeutic strategy for AS. Flavonoids have demonstrated potent antioxidant properties with potential anti-atherosclerotic effects. This study aimed to investigate the therapeutic effects of the flavonoid calycosin-7-glucoside (CG) on AS and elucidate its underlying molecular mechanisms. Methods: Macrophages were differentiated from human monocytic THP-1 cells by treatment with phorbol-12-myristate-13-acetate (PMA). Foam cell formation was induced by exposing differentiated macrophages to oxidized low-density lipoprotein (ox-LDL). Protein and inflammatory cytokine expression levels were assessed using RT-qPCR, Western blot, and ELISA assays. Total cholesterol and free cholesterol levels were quantified using commercial kits, and lipid droplet accumulation was visualized using Nile red staining. Results: Activation of activating transcription factor 1 (ATF-1) was found to mediate CG-induced suppression of inflammatory responses and foam cell formation in ox-LDL-exposed THP-1-derived macrophages. CG treatment enhanced p38 MAPK activity, which was responsible for ATF-1 activation and subsequent inhibition of inflammation and foam cell formation. Mechanistically, ATF-1 facilitated CG-induced anti-atherosclerotic effects by upregulating liver X receptor beta (LXR-β) and cystic fibrosis transmembrane conductance regulator (CFTR), which are critical for lipid metabolism and inflammation regulation, respectively. Conclusion: CG attenuates ox-LDL-induced foam cell formation and inflammatory responses in THP-1-derived macrophages by activating the p38 MAPK/ATF-1 signaling pathway, leading to the upregulation of LXR-β and CFTR. These findings highlight the potential of CG as a therapeutic agent for AS.
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