ArticleWorld journal of gastroenterology2016
Hypothalamic paraventricular nucleus stimulation reduces intestinal injury in rats with ulcerative colitis.
Article in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Deletion of Circadian Rhythms Gene BMAL1 Impairs the Intestinal Epithelial Barrier and Exacerbates Intestinal Inflammation by Inducing Pyroptosis.Mediators of inflammation · 2026Article
- A novel approach to the prevention and management of cardiovascular diseases: targeting brain-heart axis.European journal of medical research · 2025Review
- A new therapy against ulcerative colitis via the intestine and brain using the Si-based agent.Scientific reports · 2022Article
- Neuroinflammation as an etiological trigger for depression comorbid with inflammatory bowel disease.Journal of neuroinflammation · 2022Review
- Traditional Chinese medicine prescription Shenling BaiZhu powder to treat ulcerative colitis: Clinical evidence and potential mechanisms.Frontiers in pharmacology · 2022Review
- The role of inflammatory cytokines in anemia and gastrointestinal mucosal injury induced by foot electric stimulation.Scientific reports · 2021Article
- Deoxyschizandrin treats mice with ulcerative colitis possibly via the TLR4/NF-κB signaling pathway.American journal of translational research · 2021Article
- Article
- Visceral Inflammation and Immune Activation Stress the Brain.Frontiers in immunology · 2017Review
- The Vagus Nerve in the Neuro-Immune Axis: Implications in the Pathology of the Gastrointestinal Tract.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the effect and mechanism of stimulation of the hypothalamic paraventricular nucleus with glutamate acid in rats with ulcerative colitis (UC).
methodsThe rats were anesthetized with 10% chloral hydrate via abdominal injection and treated with an equal volume of TNBS + 50% ethanol enema, injected into the upper section of the anus with the tail facing up. Colonic damage scores were calculated after injecting a certain dose of glutamic acid into the paraventricular nucleus (PVN), and the effect of the nucleus tractus solitarius (NTS) and vagus nerve in alleviating UC injury through chemical stimulation of the PVN was observed in rats. Expression changes of C-myc, Apaf-1, caspase-3, interleukin (IL)-6, and IL-17 during the protection against UC injury through chemical stimulation of the PVN in rats were detected by Western blot. Malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in colon tissues of rats were measured by colorimetric methods.
resultsChemical stimulation of the PVN significantly reduced UC in rats in a dose-dependent manner. The protective effects of the chemical stimulation of the PVN on rats with UC were eliminated after chemical damage to the PVN. After glutamate receptor antagonist kynurenic acid was injected into the PVN, the protective effects of the chemical stimulation of the PVN were eliminated in rats with UC. After AVP-Vl receptor antagonist ([Deamino-penl, val4, D-Arg8]-vasopressin) was injected into NTS or bilateral chemical damage to NTS, the protective effect of the chemical stimulation of PVN on UC was also eliminated. After chemical stimulation of the PVN, SOD activity increased, MDA content decreased, C-myc protein expression significantly increased, caspase-3 and Apaf-1 protein expression significantly decreased, and IL-6 and IL-17 expression decreased in colon tissues in rats with UC.
conclusionChemical stimulation of the hypothalamic PVN provides a protective effect against UC injury in rats. Hypothalamic PVN, NTS and vagus nerve play key roles in this process.
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