Open AccessNiacin ameliorates ulcerative colitis via prostaglandin D 2 ‐mediated D prostanoid receptor 1 activation
Author(s) -
Li Juanjuan,
Kong Deping,
Wang Qi,
Wu Wei,
Tang Yanping,
Bai Tingting,
Guo Liang,
Wei Lumin,
Zhang Qianqian,
Yu Yu,
Qian Yuting,
Zuo Shengkai,
Liu Guizhu,
Liu Qian,
Wu Sheng,
Zang Yi,
Zhu Qian,
Jia Daile,
Wang Yuanyang,
Yao Weiyan,
Ji Yong,
Yin Huiyong,
Nakamura Masataka,
Lazarus Michael,
Breyer Richard M,
Wang Lifu,
Yu Ying
Publication year - 2017
Publication title -
embo molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.923
H-Index - 107
eISSN - 1757-4684
pISSN - 1757-4676
DOI - 10.15252/emmm.201606987
Subject(s) - prostanoid , ulcerative colitis , niacin , receptor , chemistry , prostaglandin , pharmacology , colitis , endocrinology , medicine , biochemistry , disease
Niacin, as an antidyslipidemic drug, elicits a strong flushing response by release of prostaglandin (PG) D 2 . However, whether niacin is beneficial for inflammatory bowel disease (IBD) remains unclear. Here, we observed niacin administration‐enhanced PGD 2 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 PGD 2 /DP1 axis. The potential efficacy of niacin in management of IBD warrants further investigation.