Abstract
BackgroundInflammatory bowel disease (IBD) is the collective term for chronic immune-mediated diseases of unknown, multifactorial etiology, arising from the interplay between genetic and environmental factors and including two main disease manifestations: ulcerative colitis (UC) and Crohn’s disease. In the last few decades, naturally occurring alkaloids have gained interest because of their substantial anti-inflammatory effects in several animal models of disease. Studies on mouse models of IBD have demonstrated the anti-inflammatory action of the main tobacco alkaloid, nicotine. In addition, anatabine, a minor tobacco alkaloid also present in peppers, tomato, and eggplant presents anti-inflammatory properties in vivo and in vitro. In this study, we aimed to evaluate the anti-inflammatory properties of nicotine and anatabine in a dextran sulfate sodium (DSS) mouse model of UC.ResultsOral administration of anatabine, but not nicotine, reduced the clinical symptoms of DSS-induced colitis. The result of gene expression analysis suggested that anatabine had a restorative effect on global DSS-induced gene expression profiles, while nicotine only had limited effects. Accordingly, MAP findings revealed that anatabine reduced the colonic abundance of DSS-associated cytokines and increased IL-10 abundance.ConclusionsOur results support the amelioration of inflammatory effects by anatabine in the DSS mouse model of UC, and suggest that anatabine constitutes a promising therapeutic agent for IBD treatment.
Highlights
Inflammatory bowel disease (IBD) is the collective term for chronic immune-mediated diseases of unknown, multifactorial etiology, arising from the interplay between genetic and environmental factors and including two main disease manifestations: ulcerative colitis (UC) and Crohn’s disease
Anatabine has a protective effect in the dextran sulfate sodium (DSS) mouse model of colitis To study the anti-inflammatory properties of nicotine and anatabine, C57BL/6 mice were provided with nicotine or anatabine in drinking water for a total of 21 days
To further follow up on the effects of nicotine and anatabine on inflammatory signaling, we evaluated the perturbation of the UC-relevant toll-like receptor (TLR)/IL-1 receptor (IL1R)/TNF receptor (TNFR)
Summary
Inflammatory bowel disease (IBD) is the collective term for chronic immune-mediated diseases of unknown, multifactorial etiology, arising from the interplay between genetic and environmental factors and including two main disease manifestations: ulcerative colitis (UC) and Crohn’s disease. In the last few decades, naturally occurring alkaloids have gained interest because of their substantial anti-inflammatory effects in several animal models of disease. Studies on mouse models of IBD have demonstrated the anti-inflammatory action of the main tobacco alkaloid, nicotine. IBD are thought to result from an inappropriate and continuing inflammatory response to commensal microbes in a genetically susceptible host. Environmental triggers such as increased hygiene, drug use, stress, smoking, and diet influence the onset of the disease [1]. The anti-inflammatory activities of plant-derived alkaloids have been documented in several animal models of disease, including respiratory distress [6], spinal cord injury [7], hepatic fibrosis [8], cancer [9], and IBD [10, 11]. The protective effects of alkaloids have been attributed to amelioration of inflammatory responses and colonic oxidative stress [12, 13], promotion of epithelial barrier function [14], and positive regulation of gut microbiota [15]
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