ABSTRACT Background Inflammatory bowel diseases, such as colitis, cause enteric nervous system dysfunction. Purinergic signaling through the P2X7 receptor (P2X7R) is activated during intestinal inflammation by extracellular ATP, but its role in chronic colitis remains unclear. Aim Investigate the effects of an experimental colitis model on the ENS from mice knockout (KO) of P2X7R. Methods Colitis was induced in wild‐type (WT) and KO mice by three cycles of Dextran Sodium Sulfate (DSS) (Cycles 1 and 2, 2% and Cycle 3, 1.5%) dissolved in drinking water for 5 days, followed by drinking water for the next 14 days (KO/DSS and WT/DSS groups). The KO/SHAM and WT/SHAM groups received water during the same period. The animals were euthanized after 57 days, and the distal colon was collected. Disease activity index and histological analysis were performed. Whole‐mount preparations of the myenteric plexus were analyzed by immunofluorescence for neuronal nitric oxide synthase (nNOS), acetylcholine transferase (ChAT), β3‐Tubulin, P2X7R, glial fibrillary acidic protein (GFAP), and S100β, and the inflammasome component NLRP3. Neuronal and glial densities were quantified. Key Results Chronic DSS‐induced colitis decreased the nitrergic and cholinergic neurons, β3‐tubulin–ir neurons, and GFAP‐ir and S100β glial cells in WT/DSS and KO/DSS groups. P2X7R‐ir cells decreased in WT/DSS animals, and NLRP3‐ir cells increased mostly in WT/DSS, indicating inflammasome activation. There were changes in neuronal profile areas. These findings were significantly attenuated in P2X7R KO mice, indicating neuronal protection during chronic inflammation. Conclusions and Inferences Experimental colitis affected the ENS of the distal colon. A slight neuronal attenuation of nNOS‐expressing neurons was observed in the P2X7RKO.
ABSTRACT Background Functional dyspepsia is a chronic gastrointestinal disorder with uncertain causes, often linked to anxiety and depression, which can worsen symptoms and hinder treatment success. Although psychological therapies and antidepressants have shown some benefit, the role of anti‐anxiety medications remains unclear. This study aims to evaluate the effectiveness of buspirone and mirtazapine in reducing symptoms and improving the quality of life for patients with functional dyspepsia. Methods In a semi experimental study, 71 patients with functional dyspepsia were randomized to receive either buspirone 15 mg, mirtazapine 7.5 mg, or pantoprazole 40 mg once daily for 12 weeks. Outcomes—anxiety severity, dyspepsia symptom score, quality of life, and adverse events—were assessed at baseline and monthly. Efficacy was analyzed by repeated‐measures ANOVA and adverse event rates by chi‐square tests. Results Both buspirone and mirtazapine significantly outperformed pantoprazole alone in reducing anxiety (buspirone vs. control at 3 months, p = 0.01; both active treatments vs. control, p < 0.05) and in alleviating functional dyspepsia symptoms by Week 12 (both vs. control, p < 0.05), with no difference between the two active drugs. Conclusions This study suggests that buspirone and mirtazapine are effective in reducing anxiety and improving symptoms in patients with functional dyspepsia. These findings highlight the potential role of anti‐anxiety medications in managing both the psychological and gastrointestinal aspects of this disorder.
