| Item type |
学術雑誌論文 / Journal Article_02(1) |
| 公開日 |
2026-01-23 |
| タイトル |
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タイトル |
Tranilast alleviates visceral hypersensitivity and colonic hyperpermeability by suppressing NLRP3 inflammasome activation in irritable bowel syndrome rat models |
|
言語 |
en |
| 言語 |
|
|
言語 |
eng |
| キーワード |
|
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主題Scheme |
Other |
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キーワード |
Gut barrier |
| キーワード |
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主題Scheme |
Other |
|
キーワード |
Irritable bowel syndrome |
| キーワード |
|
|
主題Scheme |
Other |
|
キーワード |
NLRP3 inflammasome |
| キーワード |
|
|
主題Scheme |
Other |
|
キーワード |
Tranilast |
| キーワード |
|
|
主題Scheme |
Other |
|
キーワード |
Visceral pain |
| キーワード |
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主題Scheme |
Other |
|
キーワード |
β-hydroxy butyrate |
| 資源タイプ |
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資源タイプ |
journal article |
| 著者 |
野津, 司
有江, 秀行
宮岸, 沙織
石王, 応知
高草木, 薫
奥村, 利勝
|
| bibliographic_information |
号 133,
p. 112099,
発行日 2024-05-30
|
| ISSN |
|
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収録物識別子タイプ |
PISSN |
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収録物識別子 |
1567-5769 |
| DOI |
|
|
関連タイプ |
isVersionOf |
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|
識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.1016/j.intimp.2024.112099 |
| item_1716186501932 |
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識別子タイプ |
PMID |
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関連識別子 |
38643709 |
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言語 |
en |
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|
関連名称 |
https://pubmed.ncbi.nlm.nih.gov/38643709/ |
| item_5_description_33 |
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内容記述タイプ |
Abstract |
|
内容記述 |
Visceral hypersensitivity resulting from compromised gut barrier with activated immune system is a key feature of irritable bowel syndrome (IBS). Corticotropin-releasing factor (CRF) and Toll-like receptor 4 (TLR4) activate proinflammatory cytokine signaling to induce these changes, which is one of the mechanisms of IBS. As activation of the NLRP3 inflammasome by lipopolysaccharide (LPS) or TLR4 leads to release interleukin (IL)-1β, the NLRP3 inflammasome may be involved in the pathophysiology of IBS. Tranilast, an anti-allergic drug has been demonstrated to inhibit the NLRP3 inflammasome, and we evaluated the impact of tranilast on visceral hypersensitivity and colonic hyperpermeability induced by LPS or CRF (IBS rat model). Visceral pain threshold caused by colonic balloon distention was measured by monitoring abdominal muscle contractions electrophysiologically. Colonic permeability was determined by quantifying the absorbed Evans blue within the colonic tissue. Colonic protein levels of NLRP3 and IL-1β were assessed by immunoblot or ELISA. Intragastric administration of tranilast (20-200 mg/kg) for 3 days inhibited LPS (1 mg/kg)-induced visceral hypersensitivity and colonic hyperpermeability in a dose-dependent manner. Simultaneously, tranilast also abolished these alterations induced by CRF (50 µg/kg). LPS increased colonic protein levels of NLRP3 and IL-1β, and tranilast inhibited these changes. β-hydroxy butyrate, an NLRP3 inhibitor, also abolished visceral hypersensitivity and colonic hyperpermeability caused by LPS. In contrast, IL-1β induced similar GI alterations to LPS, which were not modified by tranilast. In conclusion, tranilast improved visceral pain and colonic barrier by suppression of the NLRP3 inflammasome in IBS rat models. Tranilast may be useful for IBS treating. |
|
言語 |
en |
| 注記 |
|
|
内容記述タイプ |
Other |
|
注記 |
Copyright © 2024 Elsevier Ltd. All rights reserved |
|
言語 |
en |
| 出版タイプ |
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出版タイプ |
AM |
| item_5_textarea_42 |
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en |
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© <2024>. This manuscript version is made available under the CC-BY-NC-ND 4.0 license
https://creativecommons.org/licenses/by-nc-nd/4.0/ |
38643709.pdf (3.6 MB)
