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- MakaleYayıncıda açık erişim2026Scopus SJRQ1tVNS Mitigates Neuroinflammation and Nociception in a Rodent LPS Endotoxemia Model
Atalar, Kerem; Alim, Ece; Calikusu, Aysen; Abbasoglu Topa, Elif Gulcicek; Gok Dagidir, Hale; Bahcelioglu, Meltem; Bukan, Neslihan; Erten, Fusun; Sahin, Kazım; Akarca Dizakar, Saadet Özen
The vagus nerve plays a modulatory role in the gut-brain axis. Intestinal barrier dysfunction and lipopolysaccharide (LPS) leakage into the systemic circulation are associated with several conditions, such as irritable bowel syndrome (IBS) and migraine headache. This study investigates the impact of non-invasive transauricular vagus nerve stimulation (tVNS) on the neuroinflammatory markers and pain behavior following an acute LPS challenge. Sprague–Dawley rats (n = 28) were given LPS or vehicle and subjected to tVNS or sham intervention in an acute LPS animal model that mimics the systemic consequences of barrier dysfunction. Behaviors were evaluated at the baseline and 6 h later, complemented by testing the levels of serum and brain neuroinflammatory markers. Behavioral analyses revealed that LPS exposure reduced the time spent in the open arm, grooming duration, and periorbital mechanical pain thresholds, and increased freezing duration. The tVNS intervention reversed these behavioral changes induced by LPS. LPS administration triggered elevated serum levels of IL-6, CGRP, haptoglobin, and VE-cadherin. LPS also increased IL-1β, PAR-2, haptoglobin, CGRP, and HMGB1 levels in the brain tissue. The tVNS intervention reversed the effects observed in the brain, but it did not change the elevated levels of inflammatory molecules in the systemic circulation. tVNS has the potential to modulate neuroimmune interactions, with an early impact on the brain during LPS surge. tVNS may have potential therapeutic benefits in managing pain-related disorders associated with LPS endotoxemia.
- MakaleAçık Erişim2025Scopus SJRQ1Transauricular vagal nerve stimulation suppresses inflammatory responses in the gut and brain in an inflammatory bowel disease model
Atalar, Kerem; Alim, Ece; Yigman, Zeynep; Belen, Hayrunnisa Bolay; Erten, Fusun; Sahin, Kazım; Soylu, Ayse; Dizakar, Saadet Ozen Akarca; Bahcelioglu, Meltem
Inflammatory bowel disease (IBD) encompasses Crohn's disease (CD) and ulcerative colitis (UC), is a major health problem on a global scale and its treatment is unsatisfactory. We aimed to investigate the effects of transauricular vagal nerve stimulation (tVNS) on inflammation in rats with IBD induced by trinitrobenzene sulfonic acid (TNBS). A total of 36 adult female Sprague–Dawley rats were given TNBS, or vehicle, and tVNS, or sham, every other day for 30 min for 10 days. Postmortem macroscopic and microscopic colon morphology were evaluated by histological staining. Additionally, IL-1β, IL-6, IL-10, and TNF-α cytokine levels in the colon and the brain were evaluated by immunohistochemistry and western blotting analysis. TNBS induced epithelial damage, inflammation, ulceration, and thickened mucosal layer in the colonic tissues. Administration of tVNS significantly ameliorated the severity of TNBS-induced tissue damage and inflammatory response. TNBS also alters pro-inflammatory and anti-inflammatory balance in the brain tissue. TVNS application significantly suppressed the protein levels of pro-inflammatory cytokines, namely IL-1β, IL-6, and TNF- α while augmenting the level of anti-inflammatory cytokine IL-10 in the colonic and the brain tissue. We have shown that TNBS-mediated colonic inflammation and tissue damage are associated with neuroinflammatory responses in the brain tissue. Also demonstrated for the first time that neuroinflammatory response in the gut-brain axis is suppressed by tVNS in the IBD model. Non-invasive tVNS stands out as a new potential treatment option for types of IBD.
AtıfScopus13OpenAlex12
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