ArticleJournal of inflammation research2026
Acupoint Catgut Embedding Ameliorates Ulcerative Colitis in Association with Modulation of cGAS-STING Signaling and M1-Like/M2-Like Macrophage Markers.
Article in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: Originating from traditional acupuncture, acupoint catgut embedding (ACE) represents an integrated stimulatory therapy effective for numerous disorders. This study aims to elucidate the mechanisms underlying the protective effects of ACE against 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced ulcerative colitis (UC) in rats, focusing on cGAS-STING signaling and macrophage-associated inflammatory responses. Methods: Rats were randomly divided into four groups (n = 8) in Experiment 1 (control, model, SASP, and ACE) and Experiment 2 (control, model, ACE, and ACE + 5,6-dimethylxanthenone-4-acetic acid [DMXAA]). Integrative untargeted metabolomics and RNA sequencing were employed to explore underlying mechanisms. The expression of M1-like/M2-like macrophage markers, cGAS-STING pathway components, and epithelial barrier proteins was investigated using RT-qPCR, Western blotting, and immunofluorescence. Macrophage marker profiles were characterized by flow cytometry, and cytokine secretion was measured by ELISA. Results: ACE significantly ameliorated the DAI, colon shortening, and histological scores in UC rats. Metabolomics and RNA sequencing revealed that ACE regulated arginine metabolism and the cytosolic DNA-sensing pathway. ACE treatment was associated with decreased expression of M1-like macrophage markers and increased expression of M2-like macrophage markers, accompanied by altered inflammatory cytokine profiles in colonic tissues. Furthermore, ACE markedly suppressed the cGAS-STING pathway, as evidenced by decreased mRNA expression and protein phosphorylation of downstream molecules. Administration of the STING agonist DMXAA partially reversed ACE-associated changes in macrophage marker expression and intestinal mucosal integrity. Conclusion: ACE ameliorated TNBS-induced colitis, which was associated with reduced activation of cGAS-STING signaling and altered macrophage-associated inflammatory marker expression. This study provides a potential adjunctive therapeutic strategy for UC.
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