{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T07:26:49Z","timestamp":1782458809496,"version":"3.54.5"},"reference-count":48,"publisher":"Georg Thieme Verlag KG","issue":"08","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Drug Res (Stuttg)"],"published-print":{"date-parts":[[2022,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Inflammatory bowel disease (IBD) is an inflammatory situation involving the whole\n                    digestive system. This illness includes ulcerative colitis and Crohn\u2019s\n                    disease. According to scientific research, the immune system plays an essential\n                    part in developing this disease. Recently, buspirone has been discovered to have\n                    anti-inflammatory properties. As a result, this research aims to see if\n                    buspirone provides anti-inflammatory effects in a rat model of TNBS-induced\n                    colitis. Control, TNBS, dexamethasone (2\u2009mg\/kg), and buspirone\n                    (5, 10, and 20\u2009mg\/kg) were randomly given to six groups of 36\n                    male Wistar rats. Colitis was induced by intrarectal instillation of TNBS in all\n                    research groups except the control group, and rats were meliorated with\n                    dexamethasone and buspirone. Macroscopic and microscopic lesions appeared after\n                    colitis induction, while therapy with dexamethasone and buspirone significantly\n                    improved the lesions. TLR4 and pNF-\u03baB expression were also enhanced\n                    during colitis induction. On the other hand, the administration of dexamethasone\n                    or buspirone resulted in a considerable reduction in their expression. Tissue\n                    TNF-\u03b1 and MPO activity were enhanced after induction of colitis in terms\n                    of biochemical variables; however, administration of dexamethasone or buspirone\n                    reduced TNF-\u03b1 and MPO activity. Eventually, in an animal model of severe\n                    colitis, buspirone displayed anti-inflammatory characteristics via lowering the\n                    TLR4\/NF-\u0138B signaling pathway\u2019s activity in an animal\n                    model of acute colitis.<\/jats:p>","DOI":"10.1055\/a-1855-1491","type":"journal-article","created":{"date-parts":[[2022,7,12]],"date-time":"2022-07-12T22:59:42Z","timestamp":1657666782000},"page":"449-456","source":"Crossref","is-referenced-by-count":10,"title":["Buspirone Ameliorates Colon Inflammation in TNBS-Induced Rat Acute\n                    Colitis: The Involvement of TLR4\/NF-kB Pathway"],"prefix":"10.1055","volume":"72","author":[{"given":"Amir","family":"Rashidian","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, School of Medicine, Tehran University of\n                    Medical Sciences, Tehran, Iran"},{"name":"Experimental Medicine Research Center, Tehran University of Medical\n                    Sciences, Tehran, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sina","family":"Mohammadi","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, School of Medicine, Tehran University of\n                    Medical Sciences, Tehran, Iran"},{"name":"Experimental Medicine Research Center, Tehran University of Medical\n                    Sciences, Tehran, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amirabbas Mohammadi","family":"Hamaneh","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, School of Medicine, Tehran University of\n                    Medical Sciences, Tehran, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alireza","family":"Chaboki","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, School of Medicine, Tehran University of\n                    Medical Sciences, Tehran, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maryam","family":"Shayan","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, School of Medicine, Tehran University of\n                    Medical Sciences, Tehran, Iran"},{"name":"Experimental Medicine Research Center, Tehran University of Medical\n                    Sciences, Tehran, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohammad","family":"Sheibani","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, School of Medicine, Iran University of\n                    Medical Sciences, Tehran, Iran"},{"name":"Razi Drug Research Center, School of Medicine, Iran University of\n                    Medical Sciences, Tehran, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alireza","family":"Abdollahi","sequence":"additional","affiliation":[{"name":"Department of Pathology, School of Medicine, Tehran University of\n                    Medical Sciences, Tehran, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hasan","family":"Yousefi-Manesh","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, School of Medicine, Tehran University of\n                    Medical Sciences, Tehran, Iran"},{"name":"Experimental Medicine Research Center, Tehran University of Medical\n                    Sciences, Tehran, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ahmad Reza","family":"Dehpour","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, School of Medicine, Tehran University of\n                    Medical Sciences, Tehran, Iran"},{"name":"Experimental Medicine Research Center, Tehran University of Medical\n                    Sciences, Tehran, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"194","published-online":{"date-parts":[[2022,7,12]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","DOI":"10.1126\/sciimmunol.abc6373","article-title":"CD4+T cell activation and concomitant mTOR metabolic inhibition can\n                    ablate microbiota-specific memory cells and prevent colitis","volume":"5","author":"Q Zhao","year":"2020","journal-title":"Science Immunology"},{"key":"ref2","doi-asserted-by":"publisher","first-page":"851","DOI":"10.1007\/s10787-017-0409-1","article-title":"Foeniculum vulgare essential oil ameliorates acetic acid-induced colitis in rats\n                    through the inhibition of NF-kB pathway","volume":"26","author":"S M Rezayat","year":"2018","journal-title":"Inflammopharmacology"},{"key":"ref3","doi-asserted-by":"publisher","first-page":"275","DOI":"10.1016\/j.jphs.2014.12.016","article-title":"Involvement of stimulation of \u03b17 nicotinic acetylcholine 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ameliorates TNBS-induced colitis through\n                    S100A9\/MAPK\/NF-\u03baB signaling pathway","volume":"16","author":"Y Zhang","year":"2021","journal-title":"Chinese Medicine"},{"key":"ref7","doi-asserted-by":"publisher","first-page":"72","DOI":"10.3389\/fimmu.2018.00072","article-title":"Toll-like Receptors and Inflammatory Bowel Disease","volume":"9","author":"Y Lu","year":"2018","journal-title":"Front Immunol"},{"key":"ref8","doi-asserted-by":"publisher","first-page":"497","DOI":"10.3389\/fmicb.2020.00497","article-title":"Obacunone Protects Against Ulcerative Colitis in Mice by Modulating Gut\n                    Microbiota, Attenuating TLR4\/NF-\u03baB Signaling Cascades, and\n                    Improving Disrupted Epithelial Barriers","volume":"11","author":"X Luo","year":"2020","journal-title":"Front Microbiol"},{"key":"ref9","doi-asserted-by":"publisher","DOI":"10.1002\/kjm2.12400","article-title":"Eriodictyol attenuates TNBS-induced ulcerative colitis through 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Pharmacol"},{"key":"ref30","doi-asserted-by":"publisher","first-page":"7502","DOI":"10.1073\/pnas.95.13.7502","article-title":"Identification of novel susceptibility loci for inflammatory bowel disease on\n                    chromosomes 1p, 3q, and 4q: evidence for epistasis between 1p and IBD1","volume":"95","author":"J H Cho","year":"1998","journal-title":"Proc Natl Acad Sci U S A"},{"key":"ref31","doi-asserted-by":"publisher","first-page":"78","DOI":"10.1038\/nature07781","article-title":"Innate immune recognition of infected apoptotic cells directs T(H)17 cell\n                    differentiation","volume":"458","author":"M B Torchinsky","year":"2009","journal-title":"Nature"},{"key":"ref32","first-page":"2269","article-title":"Unique CD14+intestinal macrophages contribute to the pathogenesis of\n                    Crohn disease via IL-23\/IFN-\u03b3 axis","volume":"118","author":"N Kamada","year":"2008","journal-title":"The Journal of clinical 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