ArticleMolecular medicine (Cambridge, Mass.)2022
Protective effect of α7 nicotinic acetylcholine receptor activation on experimental colitis and its mechanism.
Article in Molecular medicine (Cambridge, Mass.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Passive smoking exposure and incidence and disease outcomes of inflammatory bowel disease: a systematic review and meta-analysis.Frontiers in public health · 2025Pooled it
- Metabolic and neuroimmune control of rheumatoid arthritis: therapeutic implications of FXR and α7-nAChR axes.Inflammopharmacology · 2026Review
- Hesperidin-loaded Eudragit S100 nanoparticles alleviate ulcerative colitis by repairing intestinal barrier and modulating gut microbiota.International journal of pharmaceutics: X · 2026Article
- Activation of α7nAChR reduces inflammation and apoptosis, promoting muscle regeneration through the AKT-FOXO1 pathway.Cell death and differentiation · 2026Article
- Activation of α7nAChR prevents maladaptive right ventricular remodeling via inhibiting the recruitment of CCR2Respiratory research · 2026Article
- Neuro-Immune Crosstalk: Molecular Mechanisms, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2026Review
- Pharmacological interventions targeting the gut-brain axis in neurological disorders: mechanisms and translational applications.Frontiers in neuroscience · 2026Review
- Gentiopicroside improves DSS-induced ulcerative colitis and secondary liver injury in mice by enhancing the intestinal barrier and regulating the gut microbiome.Scientific reports · 2025Article
- Article
- Targeting the cholinergic anti-inflammatory pathway: an innovative strategy for treating diseases.Molecular biology reports · 2025Review
- Implication of the enteric glia in the IBS-like colonic inflammation associated with endometriosis.BMC women's health · 2024Article
- Serum autoantibodies against α7-nicotinic receptors in subgroups of patients with bipolar disorder or schizophrenia: clinical features and link with peripheral inflammation.Translational psychiatry · 2024Article
- Exposing the latent phenotype of Gulf War Illness: examination of the mechanistic mediators of cognitive dysfunction.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInflammatory bowel disease (IBD) is a common chronic remitting disease with no satisfactory treatment. The aim of this study was to investigate the protective effect of α7 nicotinic acetylcholine receptor (α7nAChR), and to determine the underlying mechanism of its activity.
methodsThe expression and distribution of α7nAChR in the intestinal tissue of patients with ulcerative colitis and Crohn's disease were analyzed. The effects of vagal excitation on murine experimental colitis were investigated. The colitis model was induced in C57BL/6 mice by the administration of 3% dextran sulfate sodium (DSS). The therapeutic group received treatment with the α7nAChR agonist PNU-282987 by intraperitoneal injection.
resultsOur results showed that there was significantly increased expression of α7nAChR in colitis and Crohn's disease intestinal tissue, and its expression was mainly located in macrophages and neutrophils, which were extensively infiltrated in the disease status. Treatment with an α7nAChR agonist potently ameliorated the DSS-induced illness state, including weight loss, stool consistency, bleeding, colon shortening, and colon histological injury. α7nAChR agonist exerted anti-inflammatory effects in DSS colitis mice by suppressing the secretion of multiple types of proinflammatory factors, such as IL6, TNFα, and IL1β, and it also inhibited the colonic infiltration of inflammatory cells by blocking the DSS-induced overactivation of the NF-κB and MAPK signaling pathways. Mechanistically, activation of α7nAChR decreased the number of infiltrated M1 macrophages in the colitis intestine and inhibited the phagocytosis ability of macrophages, which were activated in response to LPS stimulation.
conclusionThus, an α7nAChR agonist ameliorated colonic pathology and inflammation in DSS-induced colitis mice by blocking the activation of inflammatory M1 macrophages.
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