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Jinyu Chen

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Open access Jul 2026

Electroacupuncture-mediated lncRNA TUG1 regulates the miR-127-3p/NF-κB p65 axis to inhibit IBS-D low-grade intestinal inflammation

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.

Kuiwu Li, Jiaojiao Wang, Ling Zou et al. · Frontiers in Immunology · 0 citations

Review Open access Aug 2026

A vicious cycle of microglial dysfunction: bridging synaptic pruning and neuroinflammation across the neurodevelopmental continuum

Rather than viewing classical neurodevelopmental disorders (NDDs) such as autism spectrum disorder (ASD) and severe psychiatric illnesses like schizophrenia (SCZ) as isolated diagnostic silos, modern biological psychiatry increasingly conceptualizes them along a shared neurodevelopmental continuum. Although altered synaptic connectivity and sustained immune dysregulation are both well-documented pathological features, the mechanistic crosstalk between them remains incompletely understood. In this review, we propose that microglia occupy a central position at the interface of these processes because of their dual roles in circuit remodeling and immune surveillance. While individual components, including complement-mediated pruning and inflammasome activation, have been extensively studied, the novelty of our framework lies in integrating these fragmented findings into a cohesive, bidirectional Dysregulated Pruning-Neuroinflammation Cycle to describe how the disruption of microglial homeostasis can sustain a self-perpetuating pathological loop. In this model, the vicious cycle may be initiated through an Outside-In route in which environmental inflammatory insults disrupt synaptic pruning, or through an Inside-Out route in which aberrant synaptic elimination releases danger signals that promote neuroinflammation. By considering early-onset ASD and adolescent/early-adult-onset SCZ, we propose that the interplay among timing, patterning, and background biases neurodevelopmental trajectories toward distinct clinical outcomes. Accordingly, this model highlights disease-modifying therapeutic strategies aimed at restoring microglial homeostasis to potentially mitigate the self-sustaining pathology in these clinically significant neurodevelopmental and psychiatric disorders.

Fan Yang, Qing Tang, Xiaofang Wang et al. · Frontiers in Immunology · 0 citations