Chronic migraine (CM) is a debilitating neurological disorder, yet the glial-specific mechanisms underlying its pathophysiology in the trigeminal nucleus caudalis (TNC)—a critical hub for craniofacial pain processing—remain poorly understood. Here, we employed single-nucleus RNA sequencing (snRNA-seq) to resolve cell-type-specific transcriptional landscapes in a nitroglycerin (NTG)-induced CM rat model, with a particular focus on microglia and astrocytes. We identified 19 transcriptional clusters representing nine major cell types, among which reactive microglia (NTG-Mic) and astrocytes (NTG-Asts) were markedly expanded. The NTG-Mic displayed a glycolysis-dominant, complement-enriched state, whereas the NTG-Asts exhibited concurrent activation of amino acid transport and cytokine signaling pathways. Pseudotime trajectory analysis revealed bifurcated glial activation paths, with NTG driving both cell types toward terminal reactive states. Intercellular communication inference uncovered suppressed homeostatic interactions (e.g., CSF1-CSF1R) alongside enhanced proinflammatory signaling (e.g., FGF1-FGFR2, PTN-SDC4), particularly affecting neuron–glia and glia–glia crosstalk. Together, these findings define a high-resolution atlas of glial reprogramming in CM, implicating state-specific metabolic–immune transitions and dysregulated glial communication as potential targets for therapeutic intervention.

Background: Hyperbaric oxygen therapy (HBOT) has been debated regarding its efficacy and safety in treating radiation enteritis (RE), with no standardized clinical protocols established. This study evaluates the clinical evidence on the use of HBOT in the management of RE, focusing on efficacy, safety, treatment parameters, and potential mechanisms.Methods: A comprehensive computer-based search was conducted across nine databases. The study assessed the effects of HBOT on gastrointestinal symptoms, immune function, inflammation, and its role in reducing the incidence of moderate to severe RE. Additionally, clinical application protocols were analyzed.Results: This study analyzed data from 22 clinical studies involving 1,318 subjects, including six RCTs incorporated into a meta-analysis. Moderate-quality evidence suggested that HBOT could significantly reduce the incidence of RE [OR = 0.32, 95% CI (0.14, 0.72), P = 0.006], particularly showing a significant advantage in decreasing the incidence of grade 3 or higher RE according to the RTOG/EORTC criteria [OR = 0.37, 95% CI (0.17, 0.82), P = 0.01]. Additionally, HBOT was shown to effectively improve gastrointestinal symptoms [MD = −1.31, 95% CI (−2.48, −0.13), P = 0.03]. Low-quality evidence suggested that HBOT reduced inflammatory markers (IL-6, CRP, TNF-α) and increased immunoglobulin levels (IgA, IgG, IgM). The most commonly reported protocol parameters were 2.0–2.5 ATA, 90–120 min per session, once daily, five times per week, for 30–40 sessions.Conclusion: This study demonstrates that HBOT effectively alleviates gastrointestinal symptoms, promotes mucosal repair, reduces inflammation, and enhances immune function in patients with RE. HBOT significantly decreases the incidence of RE, particularly severe enteritis. Optimized treatment protocols and individualized adjustments are essential for achieving optimal outcomes. Despite the potential benefits of HBOT for RE, caution is still warranted in clinical practice, with optimization of treatment protocols and individualized adjustments to ensure optimal efficacy.Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/, CRD42024618971

Purpose: Acupoint Zusanli (ST36) has been shown to reduce blood pressure, but the underlying mechanism remains unknown. This study aimed to characterize the effects of manual acupuncture (MA) at ST36 on BP and its associated mechanisms in anesthetized rats. Methods: The cardiovascular response to MA at ST36 in Sprague-Dawley rats was measured by electrocardiogram, hemodynamic methods, heart rate variability, echocardiography, laser speckle contrast imaging, and Western blotting. RNA sequencing was employed for mechanistic investigation, and validation was performed through blood enzyme-linked immunosorbent assay and pharmacologic inhibition. Results: Stimulation of ST36 increased peripheral blood flow while decreasing the velocity time integral of the femoral artery and cardiac stroke volume. This stimulation induced transient hypotension, accompanied by a decreased heart rate and reduced cardiac contractility, thereby exerting negative chronotropic and inotropic effects on the heart. Furthermore, the increased low-/high-frequency ratio after ST36 stimulation, along with the upregulation of phosphorylated tyrosine hydroxylase, indicated sympathetic activation. RNA sequencing at the local acupoint revealed enrichment of inflammation-related pathways following ST36 stimulation, which was corroborated by elevated tumor necrosis factor-alpha (TNF-α) levels in the serum. Notably, the nitric oxide synthase (NOS) inhibitor L-NG-Nitro arginine methyl ester (L-NAME) effectively suppressed the induced hypotension. Conclusion: These results indicated that MA at ST36 induced inflammation, which activated NOS and resulted in the release of nitric oxide. This led to the vasodilation of peripheral vessels and transient hypotension.