ArticleFrontiers in immunology2026
Electroacupuncture-mediated lncRNA TUG1 regulates the miR-127-3p/NF-κB p65 axis to inhibit IBS-D low-grade intestinal inflammation.
Article in Frontiers in immunology, 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
Background: Electroacupuncture (EA) demonstrates efficacy in alleviating diarrhea-predominant irritable bowel syndrome (IBS-D), yet its mechanisms concerning low-grade intestinal inflammation remain insufficiently elucidated. This study investigated whether EA ameliorates IBS-D symptoms by modulating the long non-coding RNA Taurine Upregulated Gene 1 (lncRNA TUG1)/microRNA-127 -3p (miR-127-3p)/nuclear factor-kappa B p65 (NF-κB p65) axis. Methods: An IBS-D rat model was established using maternal separation, acetic acid enema, and chronic restraint stress. Rats were randomly allocated into control, model, EA (at ST-25 and ST-37), drug (rifaximin), and PDTC (NF-κB p65 inhibitor) groups. Behavioral assessments (body weight, loose stool rate, abdominal withdrawal reflex) were conducted. Molecular analyses included dual-luciferase reporter assays, RT-qPCR, western blot, ELISA, and immunofluorescence to evaluate the TUG1/miR-127-3p/NF-κB p65 axis, inflammatory factors (TNF-α, NLRP3, IL-6), and tight junction proteins (occludin, claudin-1, ZO-1). Intestinal ultrastructure was examined by electron microscopy. Results: EA significantly improved general status, reduced diarrhea and visceral hypersensitivity in IBS-D rats, comparable to rifaximin and PDTC. Mechanistically, EA upregulated colonic lncRNA TUG1 expression, which sequesters miR-127-3p and partially derepresses NF-κB negative regulators (IκBα, A20), consistent with attenuated NF-κB pathway activation. This was associated with downregulated downstream pro-inflammatory mediators (NF-κB p65, TNF-α, NLRP3, IL-6) in serum and colon tissues. Furthermore, EA restored intestinal barrier integrity, as evidenced by improved mucosal ultrastructure and increased expression of tight junction proteins. Conclusion: EA alleviates low-grade intestinal inflammation and visceral hypersensitivity in IBS-D rats. The therapeutic effect is mediated, at least in part through upregulation of lncRNA TUG1, which sponges miR-127-3p to inhibit the NF-κB p65 signaling pathway, thereby reducing inflammatory cytokine release and repairing the intestinal epithelial barrier. These findings suggest the TUG1/miR-127/NF-κB axis as a candidate therapeutic target for EA in IBS-D.
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