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Abstract
Niacin, as an antidyslipidemic drug, elicits a strong flushing response by release of prostaglandin (PG) D2. However, whether niacin is beneficial for inflammatory bowel disease (IBD) remains unclear. Here, we observed niacin administration‐enhanced PGD2 production in colon tissues in dextran sulfate sodium (DSS)‐challenged mice, and protected mice against DSS or 2,4,6‐trinitrobenzene sulfonic acid (TNBS)‐induced colitis in D prostanoid receptor 1 (DP1)‐dependent manner. Specific ablation of DP1 receptor in vascular endothelial cells, colonic epithelium, and myeloid cells augmented DSS/TNBS‐induced colitis in mice through increasing vascular permeability, promoting apoptosis of epithelial cells, and stimulating pro‐inflammatory cytokine secretion of macrophages, respectively. Niacin treatment improved vascular permeability, reduced apoptotic epithelial cells, promoted epithelial cell update, and suppressed pro‐inflammatory gene expression of macrophages. Moreover, treatment with niacin‐containing retention enema effectively promoted UC clinical remission and mucosal healing in patients with moderately active disease. Therefore, niacin displayed multiple beneficial effects on DSS/TNBS‐induced colitis in mice by activation of PGD2/DP1 axis. The potential efficacy of niacin in management of IBD warrants further investigation.
Highlights
Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) characterized by recurrent episodes of active disease, which commonly affects the colon, the rectum, or both simultaneously
To explore whether niacin protects against inflammatory bowel diseases (IBDs) through releasing prostaglandin D2 (PGD2), we first examined niacin-induced PGD2 production in colon tissues and urinary secretion of PGD2 metabolites- 11,15-Dioxo-9a-hydroxy-2,3,4,5-tetranorprostan-1,20-dioic acid from dextran sulfate sodium (DSS)-induced colitis mouse model by using mass spectrometry analysis
We demonstrated that niacin displayed multifaceted protective effects against DSS/ trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice through activation of the D prostanoid receptor 1 (DP1) receptor, including inhibition of vascular leakage, suppression of
Summary
Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) characterized by recurrent episodes of active disease, which commonly affects the colon, the rectum, or both simultaneously. Genome-wide association studies (GWAS) have identified 47 genetic susceptibility loci for UC, 28 of which are shared between Crohn’s disease (CD) and UC (Franke et al, 2010; Anderson et al, 2011). These risk loci implicated in IBD are involved in different key signal pathways which are essential for intestinal homeostasis, such as epithelial restitution, barrier function, innate and adaptive immune regulation, microbial defense, cellular stress, and metabolism (Khor et al, 2011).
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