Niacin ameliorates ulcerative colitis via prostaglandin D2‐mediated D prostanoid receptor 1 activation
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 dextr...
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Springer Nature
2017-03-01
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| Series: | EMBO Molecular Medicine |
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| Online Access: | https://doi.org/10.15252/emmm.201606987 |
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| author | Juanjuan Li Deping Kong Qi Wang Wei Wu Yanping Tang Tingting Bai Liang Guo Lumin Wei Qianqian Zhang Yu Yu Yuting Qian Shengkai Zuo Guizhu Liu Qian Liu Sheng Wu Yi Zang Qian Zhu Daile Jia Yuanyang Wang Weiyan Yao Yong Ji Huiyong Yin Masataka Nakamura Michael Lazarus Richard M Breyer Lifu Wang Ying Yu |
| author_facet | Juanjuan Li Deping Kong Qi Wang Wei Wu Yanping Tang Tingting Bai Liang Guo Lumin Wei Qianqian Zhang Yu Yu Yuting Qian Shengkai Zuo Guizhu Liu Qian Liu Sheng Wu Yi Zang Qian Zhu Daile Jia Yuanyang Wang Weiyan Yao Yong Ji Huiyong Yin Masataka Nakamura Michael Lazarus Richard M Breyer Lifu Wang Ying Yu |
| author_sort | Juanjuan Li |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-b98e9055c3c040d48995bb25f39bd9ab |
| institution | Kabale University |
| issn | 1757-4676 1757-4684 |
| language | English |
| publishDate | 2017-03-01 |
| publisher | Springer Nature |
| record_format | Article |
| series | EMBO Molecular Medicine |
| spelling | doaj-art-b98e9055c3c040d48995bb25f39bd9ab2025-08-20T04:03:07ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842017-03-019557158810.15252/emmm.201606987Niacin ameliorates ulcerative colitis via prostaglandin D2‐mediated D prostanoid receptor 1 activationJuanjuan Li0Deping Kong1Qi Wang2Wei Wu3Yanping Tang4Tingting Bai5Liang Guo6Lumin Wei7Qianqian Zhang8Yu Yu9Yuting Qian10Shengkai Zuo11Guizhu Liu12Qian Liu13Sheng Wu14Yi Zang15Qian Zhu16Daile Jia17Yuanyang Wang18Weiyan Yao19Yong Ji20Huiyong Yin21Masataka Nakamura22Michael Lazarus23Richard M Breyer24Lifu Wang25Ying Yu26Department of Gastroenterology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of MedicineKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of SciencesDepartment of Gastroenterology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of MedicineDepartment of Gastroenterology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of MedicineDepartment of Gastroenterology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of MedicineDepartment of Gastroenterology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of MedicineDepartment of Breast Surgery, Breast Cancer Institute, Fudan University Shanghai Cancer CenterDepartment of Gastroenterology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of MedicineKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of SciencesKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of SciencesDepartment of Gastroenterology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of MedicineKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of SciencesKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of SciencesKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of SciencesDepartment of Gastroenterology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of MedicineDepartment of Gastroenterology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of MedicineKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of SciencesKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of SciencesDepartment of Pharmacology, School of Basic Medical Sciences, Tianjin Medical UniversityDepartment of Gastroenterology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of MedicineThe Key Laboratory of Cardiovascular Disease and Molecular Intervention, Atherosclerosis Research Centre, Nanjing Medical University, NanjingKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of SciencesHuman Gene Sciences Center, Tokyo Medical and Dental University, Bunkyo‐kuInternational Institute for Integrative Sleep Medicine (WPI‐IIIS), University of Tsukuba, Tsukuba CityDepartment of Veterans Affairs, Tennessee Valley Health AuthorityDepartment of Gastroenterology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of MedicineKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of SciencesAbstract 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.https://doi.org/10.15252/emmm.201606987DP1 receptorniacinprostaglandinretention enemaulcerative colitis |
| spellingShingle | Juanjuan Li Deping Kong Qi Wang Wei Wu Yanping Tang Tingting Bai Liang Guo Lumin Wei Qianqian Zhang Yu Yu Yuting Qian Shengkai Zuo Guizhu Liu Qian Liu Sheng Wu Yi Zang Qian Zhu Daile Jia Yuanyang Wang Weiyan Yao Yong Ji Huiyong Yin Masataka Nakamura Michael Lazarus Richard M Breyer Lifu Wang Ying Yu Niacin ameliorates ulcerative colitis via prostaglandin D2‐mediated D prostanoid receptor 1 activation EMBO Molecular Medicine DP1 receptor niacin prostaglandin retention enema ulcerative colitis |
| title | Niacin ameliorates ulcerative colitis via prostaglandin D2‐mediated D prostanoid receptor 1 activation |
| title_full | Niacin ameliorates ulcerative colitis via prostaglandin D2‐mediated D prostanoid receptor 1 activation |
| title_fullStr | Niacin ameliorates ulcerative colitis via prostaglandin D2‐mediated D prostanoid receptor 1 activation |
| title_full_unstemmed | Niacin ameliorates ulcerative colitis via prostaglandin D2‐mediated D prostanoid receptor 1 activation |
| title_short | Niacin ameliorates ulcerative colitis via prostaglandin D2‐mediated D prostanoid receptor 1 activation |
| title_sort | niacin ameliorates ulcerative colitis via prostaglandin d2 mediated d prostanoid receptor 1 activation |
| topic | DP1 receptor niacin prostaglandin retention enema ulcerative colitis |
| url | https://doi.org/10.15252/emmm.201606987 |
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