Niacin ameliorates ulcerative colitis via prostaglandin $ D_{2} $‐mediated D prostanoid receptor 1 activation
Abstract 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 ti...
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Gespeichert in:
| Autor*in: |
Li, Juanjuan [verfasserIn] Kong, Deping [verfasserIn] Wang, Qi [verfasserIn] Wu, Wei [verfasserIn] Tang, Yanping [verfasserIn] Bai, Tingting [verfasserIn] Guo, Liang [verfasserIn] Wei, Lumin [verfasserIn] Zhang, Qianqian [verfasserIn] Yu, Yu [verfasserIn] Qian, Yuting [verfasserIn] Zuo, Shengkai [verfasserIn] Liu, Guizhu [verfasserIn] Liu, Qian [verfasserIn] Wu, Sheng [verfasserIn] Zang, Yi [verfasserIn] Zhu, Qian [verfasserIn] Jia, Daile [verfasserIn] Wang, Yuanyang [verfasserIn] Yao, Weiyan [verfasserIn] Ji, Yong [verfasserIn] Yin, Huiyong [verfasserIn] Nakamura, Masataka [verfasserIn] Lazarus, Michael [verfasserIn] Breyer, Richard M [verfasserIn] Wang, Lifu [verfasserIn] Yu, Ying [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017 |
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© The Authors. Published under the terms of the CC BY 4.0 license 2017 |
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| Übergeordnetes Werk: |
Enthalten in: EMBO Molecular Medicine - Nature Publishing Group UK, 2023, 9(2017), 5 vom: 27. März, Seite 571-588 |
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| Übergeordnetes Werk: |
volume:9 ; year:2017 ; number:5 ; day:27 ; month:03 ; pages:571-588 |
| Links: |
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| DOI / URN: |
10.15252/emmm.201606987 |
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SPR057909113 |
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| 245 | 1 | 0 | |a Niacin ameliorates ulcerative colitis via prostaglandin $ D_{2} $‐mediated D prostanoid receptor 1 activation |
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| 520 | |a Abstract 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. | ||
| 520 | |a Synopsis Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. Niacin increases $ PGD_{2} $ release in both mice and humans.Niacin confers protection against DSS/TNBS‐induced colitis in mice through DP1‐mediated inhibition of vascular leakage, suppression of colonic epithelium apoptosis, and reduction of pro‐inflammatory cytokine secretion.Retention enema treatment containing niacin effectively promotes clinical remission and mucosal healing in patients with moderately active UC. | ||
| 520 | |a Graphical Abstract Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. | ||
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10.15252/emmm.201606987 doi (DE-627)SPR057909113 (SPR)emmm.201606987-e DE-627 ger DE-627 rakwb eng Li, Juanjuan verfasserin aut Niacin ameliorates ulcerative colitis via prostaglandin $ D_{2} $‐mediated D prostanoid receptor 1 activation 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Authors. Published under the terms of the CC BY 4.0 license 2017 Abstract 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. Synopsis Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. Niacin increases $ PGD_{2} $ release in both mice and humans.Niacin confers protection against DSS/TNBS‐induced colitis in mice through DP1‐mediated inhibition of vascular leakage, suppression of colonic epithelium apoptosis, and reduction of pro‐inflammatory cytokine secretion.Retention enema treatment containing niacin effectively promotes clinical remission and mucosal healing in patients with moderately active UC. Graphical Abstract Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. DP1 receptor (dpeaa)DE-He213 niacin (dpeaa)DE-He213 prostaglandin (dpeaa)DE-He213 retention enema (dpeaa)DE-He213 ulcerative colitis (dpeaa)DE-He213 Kong, Deping verfasserin aut Wang, Qi verfasserin aut Wu, Wei verfasserin aut Tang, Yanping verfasserin aut Bai, Tingting verfasserin aut Guo, Liang verfasserin aut Wei, Lumin verfasserin aut Zhang, Qianqian verfasserin aut Yu, Yu verfasserin aut Qian, Yuting verfasserin aut Zuo, Shengkai verfasserin aut Liu, Guizhu verfasserin aut Liu, Qian verfasserin aut Wu, Sheng verfasserin aut Zang, Yi verfasserin aut Zhu, Qian verfasserin aut Jia, Daile verfasserin aut Wang, Yuanyang verfasserin aut Yao, Weiyan verfasserin aut Ji, Yong verfasserin aut Yin, Huiyong verfasserin aut Nakamura, Masataka verfasserin aut Lazarus, Michael verfasserin aut Breyer, Richard M verfasserin aut Wang, Lifu verfasserin (orcid)0000-0001-5172-9932 aut Yu, Ying verfasserin (orcid)0000-0002-6476-1752 aut Enthalten in EMBO Molecular Medicine Nature Publishing Group UK, 2023 9(2017), 5 vom: 27. März, Seite 571-588 (DE-627)594772761 (DE-600)2485479-7 1757-4684 nnns volume:9 year:2017 number:5 day:27 month:03 pages:571-588 https://dx.doi.org/10.15252/emmm.201606987 X:SPRINGER Resolving-System kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 9 2017 5 27 03 571-588 |
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10.15252/emmm.201606987 doi (DE-627)SPR057909113 (SPR)emmm.201606987-e DE-627 ger DE-627 rakwb eng Li, Juanjuan verfasserin aut Niacin ameliorates ulcerative colitis via prostaglandin $ D_{2} $‐mediated D prostanoid receptor 1 activation 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Authors. Published under the terms of the CC BY 4.0 license 2017 Abstract 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. Synopsis Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. Niacin increases $ PGD_{2} $ release in both mice and humans.Niacin confers protection against DSS/TNBS‐induced colitis in mice through DP1‐mediated inhibition of vascular leakage, suppression of colonic epithelium apoptosis, and reduction of pro‐inflammatory cytokine secretion.Retention enema treatment containing niacin effectively promotes clinical remission and mucosal healing in patients with moderately active UC. Graphical Abstract Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. DP1 receptor (dpeaa)DE-He213 niacin (dpeaa)DE-He213 prostaglandin (dpeaa)DE-He213 retention enema (dpeaa)DE-He213 ulcerative colitis (dpeaa)DE-He213 Kong, Deping verfasserin aut Wang, Qi verfasserin aut Wu, Wei verfasserin aut Tang, Yanping verfasserin aut Bai, Tingting verfasserin aut Guo, Liang verfasserin aut Wei, Lumin verfasserin aut Zhang, Qianqian verfasserin aut Yu, Yu verfasserin aut Qian, Yuting verfasserin aut Zuo, Shengkai verfasserin aut Liu, Guizhu verfasserin aut Liu, Qian verfasserin aut Wu, Sheng verfasserin aut Zang, Yi verfasserin aut Zhu, Qian verfasserin aut Jia, Daile verfasserin aut Wang, Yuanyang verfasserin aut Yao, Weiyan verfasserin aut Ji, Yong verfasserin aut Yin, Huiyong verfasserin aut Nakamura, Masataka verfasserin aut Lazarus, Michael verfasserin aut Breyer, Richard M verfasserin aut Wang, Lifu verfasserin (orcid)0000-0001-5172-9932 aut Yu, Ying verfasserin (orcid)0000-0002-6476-1752 aut Enthalten in EMBO Molecular Medicine Nature Publishing Group UK, 2023 9(2017), 5 vom: 27. März, Seite 571-588 (DE-627)594772761 (DE-600)2485479-7 1757-4684 nnns volume:9 year:2017 number:5 day:27 month:03 pages:571-588 https://dx.doi.org/10.15252/emmm.201606987 X:SPRINGER Resolving-System kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 9 2017 5 27 03 571-588 |
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10.15252/emmm.201606987 doi (DE-627)SPR057909113 (SPR)emmm.201606987-e DE-627 ger DE-627 rakwb eng Li, Juanjuan verfasserin aut Niacin ameliorates ulcerative colitis via prostaglandin $ D_{2} $‐mediated D prostanoid receptor 1 activation 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Authors. Published under the terms of the CC BY 4.0 license 2017 Abstract 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. Synopsis Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. Niacin increases $ PGD_{2} $ release in both mice and humans.Niacin confers protection against DSS/TNBS‐induced colitis in mice through DP1‐mediated inhibition of vascular leakage, suppression of colonic epithelium apoptosis, and reduction of pro‐inflammatory cytokine secretion.Retention enema treatment containing niacin effectively promotes clinical remission and mucosal healing in patients with moderately active UC. Graphical Abstract Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. DP1 receptor (dpeaa)DE-He213 niacin (dpeaa)DE-He213 prostaglandin (dpeaa)DE-He213 retention enema (dpeaa)DE-He213 ulcerative colitis (dpeaa)DE-He213 Kong, Deping verfasserin aut Wang, Qi verfasserin aut Wu, Wei verfasserin aut Tang, Yanping verfasserin aut Bai, Tingting verfasserin aut Guo, Liang verfasserin aut Wei, Lumin verfasserin aut Zhang, Qianqian verfasserin aut Yu, Yu verfasserin aut Qian, Yuting verfasserin aut Zuo, Shengkai verfasserin aut Liu, Guizhu verfasserin aut Liu, Qian verfasserin aut Wu, Sheng verfasserin aut Zang, Yi verfasserin aut Zhu, Qian verfasserin aut Jia, Daile verfasserin aut Wang, Yuanyang verfasserin aut Yao, Weiyan verfasserin aut Ji, Yong verfasserin aut Yin, Huiyong verfasserin aut Nakamura, Masataka verfasserin aut Lazarus, Michael verfasserin aut Breyer, Richard M verfasserin aut Wang, Lifu verfasserin (orcid)0000-0001-5172-9932 aut Yu, Ying verfasserin (orcid)0000-0002-6476-1752 aut Enthalten in EMBO Molecular Medicine Nature Publishing Group UK, 2023 9(2017), 5 vom: 27. März, Seite 571-588 (DE-627)594772761 (DE-600)2485479-7 1757-4684 nnns volume:9 year:2017 number:5 day:27 month:03 pages:571-588 https://dx.doi.org/10.15252/emmm.201606987 X:SPRINGER Resolving-System kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 9 2017 5 27 03 571-588 |
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10.15252/emmm.201606987 doi (DE-627)SPR057909113 (SPR)emmm.201606987-e DE-627 ger DE-627 rakwb eng Li, Juanjuan verfasserin aut Niacin ameliorates ulcerative colitis via prostaglandin $ D_{2} $‐mediated D prostanoid receptor 1 activation 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Authors. Published under the terms of the CC BY 4.0 license 2017 Abstract 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. Synopsis Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. Niacin increases $ PGD_{2} $ release in both mice and humans.Niacin confers protection against DSS/TNBS‐induced colitis in mice through DP1‐mediated inhibition of vascular leakage, suppression of colonic epithelium apoptosis, and reduction of pro‐inflammatory cytokine secretion.Retention enema treatment containing niacin effectively promotes clinical remission and mucosal healing in patients with moderately active UC. Graphical Abstract Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. DP1 receptor (dpeaa)DE-He213 niacin (dpeaa)DE-He213 prostaglandin (dpeaa)DE-He213 retention enema (dpeaa)DE-He213 ulcerative colitis (dpeaa)DE-He213 Kong, Deping verfasserin aut Wang, Qi verfasserin aut Wu, Wei verfasserin aut Tang, Yanping verfasserin aut Bai, Tingting verfasserin aut Guo, Liang verfasserin aut Wei, Lumin verfasserin aut Zhang, Qianqian verfasserin aut Yu, Yu verfasserin aut Qian, Yuting verfasserin aut Zuo, Shengkai verfasserin aut Liu, Guizhu verfasserin aut Liu, Qian verfasserin aut Wu, Sheng verfasserin aut Zang, Yi verfasserin aut Zhu, Qian verfasserin aut Jia, Daile verfasserin aut Wang, Yuanyang verfasserin aut Yao, Weiyan verfasserin aut Ji, Yong verfasserin aut Yin, Huiyong verfasserin aut Nakamura, Masataka verfasserin aut Lazarus, Michael verfasserin aut Breyer, Richard M verfasserin aut Wang, Lifu verfasserin (orcid)0000-0001-5172-9932 aut Yu, Ying verfasserin (orcid)0000-0002-6476-1752 aut Enthalten in EMBO Molecular Medicine Nature Publishing Group UK, 2023 9(2017), 5 vom: 27. März, Seite 571-588 (DE-627)594772761 (DE-600)2485479-7 1757-4684 nnns volume:9 year:2017 number:5 day:27 month:03 pages:571-588 https://dx.doi.org/10.15252/emmm.201606987 X:SPRINGER Resolving-System kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 9 2017 5 27 03 571-588 |
| allfieldsSound |
10.15252/emmm.201606987 doi (DE-627)SPR057909113 (SPR)emmm.201606987-e DE-627 ger DE-627 rakwb eng Li, Juanjuan verfasserin aut Niacin ameliorates ulcerative colitis via prostaglandin $ D_{2} $‐mediated D prostanoid receptor 1 activation 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Authors. Published under the terms of the CC BY 4.0 license 2017 Abstract 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. Synopsis Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. Niacin increases $ PGD_{2} $ release in both mice and humans.Niacin confers protection against DSS/TNBS‐induced colitis in mice through DP1‐mediated inhibition of vascular leakage, suppression of colonic epithelium apoptosis, and reduction of pro‐inflammatory cytokine secretion.Retention enema treatment containing niacin effectively promotes clinical remission and mucosal healing in patients with moderately active UC. Graphical Abstract Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. DP1 receptor (dpeaa)DE-He213 niacin (dpeaa)DE-He213 prostaglandin (dpeaa)DE-He213 retention enema (dpeaa)DE-He213 ulcerative colitis (dpeaa)DE-He213 Kong, Deping verfasserin aut Wang, Qi verfasserin aut Wu, Wei verfasserin aut Tang, Yanping verfasserin aut Bai, Tingting verfasserin aut Guo, Liang verfasserin aut Wei, Lumin verfasserin aut Zhang, Qianqian verfasserin aut Yu, Yu verfasserin aut Qian, Yuting verfasserin aut Zuo, Shengkai verfasserin aut Liu, Guizhu verfasserin aut Liu, Qian verfasserin aut Wu, Sheng verfasserin aut Zang, Yi verfasserin aut Zhu, Qian verfasserin aut Jia, Daile verfasserin aut Wang, Yuanyang verfasserin aut Yao, Weiyan verfasserin aut Ji, Yong verfasserin aut Yin, Huiyong verfasserin aut Nakamura, Masataka verfasserin aut Lazarus, Michael verfasserin aut Breyer, Richard M verfasserin aut Wang, Lifu verfasserin (orcid)0000-0001-5172-9932 aut Yu, Ying verfasserin (orcid)0000-0002-6476-1752 aut Enthalten in EMBO Molecular Medicine Nature Publishing Group UK, 2023 9(2017), 5 vom: 27. März, Seite 571-588 (DE-627)594772761 (DE-600)2485479-7 1757-4684 nnns volume:9 year:2017 number:5 day:27 month:03 pages:571-588 https://dx.doi.org/10.15252/emmm.201606987 X:SPRINGER Resolving-System kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 9 2017 5 27 03 571-588 |
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Enthalten in EMBO Molecular Medicine 9(2017), 5 vom: 27. März, Seite 571-588 volume:9 year:2017 number:5 day:27 month:03 pages:571-588 |
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Enthalten in EMBO Molecular Medicine 9(2017), 5 vom: 27. März, Seite 571-588 volume:9 year:2017 number:5 day:27 month:03 pages:571-588 |
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DP1 receptor niacin prostaglandin retention enema ulcerative colitis |
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Li, Juanjuan @@aut@@ Kong, Deping @@aut@@ Wang, Qi @@aut@@ Wu, Wei @@aut@@ Tang, Yanping @@aut@@ Bai, Tingting @@aut@@ Guo, Liang @@aut@@ Wei, Lumin @@aut@@ Zhang, Qianqian @@aut@@ Yu, Yu @@aut@@ Qian, Yuting @@aut@@ Zuo, Shengkai @@aut@@ Liu, Guizhu @@aut@@ Liu, Qian @@aut@@ Wu, Sheng @@aut@@ Zang, Yi @@aut@@ Zhu, Qian @@aut@@ Jia, Daile @@aut@@ Wang, Yuanyang @@aut@@ Yao, Weiyan @@aut@@ Ji, Yong @@aut@@ Yin, Huiyong @@aut@@ Nakamura, Masataka @@aut@@ Lazarus, Michael @@aut@@ Breyer, Richard M @@aut@@ Wang, Lifu @@aut@@ Yu, Ying @@aut@@ |
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2017-03-27T00:00:00Z |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000naa a22002652 4500</leader><controlfield tag="001">SPR057909113</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20241019064943.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">241019s2017 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.15252/emmm.201606987</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR057909113</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)emmm.201606987-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Li, Juanjuan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Niacin ameliorates ulcerative colitis via prostaglandin $ D_{2} $‐mediated D prostanoid receptor 1 activation</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2017</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© The Authors. Published under the terms of the CC BY 4.0 license 2017</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract 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.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Synopsis Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. Niacin increases $ PGD_{2} $ release in both mice and humans.Niacin confers protection against DSS/TNBS‐induced colitis in mice through DP1‐mediated inhibition of vascular leakage, suppression of colonic epithelium apoptosis, and reduction of pro‐inflammatory cytokine secretion.Retention enema treatment containing niacin effectively promotes clinical remission and mucosal healing in patients with moderately active UC.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Graphical Abstract Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. 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|
| author |
Li, Juanjuan |
| spellingShingle |
Li, Juanjuan misc DP1 receptor misc niacin misc prostaglandin misc retention enema misc ulcerative colitis Niacin ameliorates ulcerative colitis via prostaglandin $ D_{2} $‐mediated D prostanoid receptor 1 activation |
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Li, Juanjuan |
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electronic Article |
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keep |
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aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut |
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springer |
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true |
| illustrated |
Not Illustrated |
| issn |
1757-4684 |
| topic_title |
Niacin ameliorates ulcerative colitis via prostaglandin $ D_{2} $‐mediated D prostanoid receptor 1 activation DP1 receptor (dpeaa)DE-He213 niacin (dpeaa)DE-He213 prostaglandin (dpeaa)DE-He213 retention enema (dpeaa)DE-He213 ulcerative colitis (dpeaa)DE-He213 |
| topic |
misc DP1 receptor misc niacin misc prostaglandin misc retention enema misc ulcerative colitis |
| topic_unstemmed |
misc DP1 receptor misc niacin misc prostaglandin misc retention enema misc ulcerative colitis |
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Niacin ameliorates ulcerative colitis via prostaglandin $ D_{2} $‐mediated D prostanoid receptor 1 activation |
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Niacin ameliorates ulcerative colitis via prostaglandin $ D_{2} $‐mediated D prostanoid receptor 1 activation |
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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 |
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niacin ameliorates ulcerative colitis via prostaglandin $ d_{2} $‐mediated d prostanoid receptor 1 activation |
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Niacin ameliorates ulcerative colitis via prostaglandin $ D_{2} $‐mediated D prostanoid receptor 1 activation |
| abstract |
Abstract 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. Synopsis Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. Niacin increases $ PGD_{2} $ release in both mice and humans.Niacin confers protection against DSS/TNBS‐induced colitis in mice through DP1‐mediated inhibition of vascular leakage, suppression of colonic epithelium apoptosis, and reduction of pro‐inflammatory cytokine secretion.Retention enema treatment containing niacin effectively promotes clinical remission and mucosal healing in patients with moderately active UC. Graphical Abstract Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. © The Authors. Published under the terms of the CC BY 4.0 license 2017 |
| abstractGer |
Abstract 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. Synopsis Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. Niacin increases $ PGD_{2} $ release in both mice and humans.Niacin confers protection against DSS/TNBS‐induced colitis in mice through DP1‐mediated inhibition of vascular leakage, suppression of colonic epithelium apoptosis, and reduction of pro‐inflammatory cytokine secretion.Retention enema treatment containing niacin effectively promotes clinical remission and mucosal healing in patients with moderately active UC. Graphical Abstract Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. © The Authors. Published under the terms of the CC BY 4.0 license 2017 |
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Abstract 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. Synopsis Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. Niacin increases $ PGD_{2} $ release in both mice and humans.Niacin confers protection against DSS/TNBS‐induced colitis in mice through DP1‐mediated inhibition of vascular leakage, suppression of colonic epithelium apoptosis, and reduction of pro‐inflammatory cytokine secretion.Retention enema treatment containing niacin effectively promotes clinical remission and mucosal healing in patients with moderately active UC. Graphical Abstract Niacin, an ancient lipid‐lowering drug that elicits a strong flushing response through release of prostaglandin (PG) $ D_{2} $. Niacin improves experimentally induced ulcerative colitis in mice and humans through the activation of $ PGD_{2} $/DP1 axis. © The Authors. Published under the terms of the CC BY 4.0 license 2017 |
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| score |
7.398917 |