| Item type |
学術雑誌論文 / Journal Article_02(1) |
| 公開日 |
2025-04-18 |
| タイトル |
|
|
タイトル |
Phlorizin attenuates visceral hypersensitivity and colonic hyperpermeability in a rat model of irritable bowel syndrome |
|
言語 |
en |
| 言語 |
|
|
言語 |
eng |
| キーワード |
|
|
主題Scheme |
Other |
|
キーワード |
Gut barrier |
| キーワード |
|
|
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 |
Sodium-linked glucose transporter |
| キーワード |
|
|
主題Scheme |
Other |
|
キーワード |
Visceral sensation |
| 資源タイプ |
|
|
資源タイプ |
journal article |
| アクセス権 |
|
|
アクセス権 |
open access |
|
アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
| 著者 |
野津, 司
宮岸, 沙織
石王, 応知
高草木, 薫
奥村, 利勝
|
| bibliographic_information |
en : Biomedicine and Pharmacotherapy
巻 139,
p. 111649,
発行日 2021-07-01
|
| ISSN |
|
|
収録物識別子タイプ |
PISSN |
|
収録物識別子 |
0753-3322 |
| DOI |
|
|
関連タイプ |
isVersionOf |
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.1016/j.biopha.2021.111649 |
| item_1716186501932 |
|
|
|
識別子タイプ |
PMID |
|
|
関連識別子 |
33957565 |
| item_5_description_33 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
Visceral hypersensitivity and impaired gut barrier are crucial contributors to the pathophysiology of irritable bowel syndrome (IBS), and those are mediated via corticotropin-releasing factor (CRF)-Toll like receptor 4-pro-inflammatory cytokine signaling. Phlorizin is an inhibitor of sodium-linked glucose transporters (SGLTs), and known to have anti-cytokine properties. Thus, we hypothesized that phlorizin may improve these gastrointestinal changes in IBS, and tested this hypothesis in rat IBS models, i.e., lipopolysaccharide (LPS) or CRF-induced visceral hypersensitivity and colonic hyperpermeability. The visceral pain threshold in response to colonic balloon distention was estimated by abdominal muscle contractions by electromyogram, and colonic permeability was measured by quantifying the absorbed Evans blue in colonic tissue. Subcutaneous (s.c.) injection of phlorizin inhibited visceral hypersensitivity and colonic hyperpermeability induced by LPS in a dose-dependent manner. Phlorizin also blocked CRF-induced these gastrointestinal changes. Phlorizin is known to inhibit both SGLT1 and SGLT2, but intragastric administration of phlorizin may only inhibit SGLT1 because gut mainly expresses SGLT1. We found that intragastric phlorizin did not display any effects, but ipragliflozin, an orally active and selective SGLT2 inhibitor improved the gastrointestinal changes in the LPS model. Compound C, an adenosine monophosphate-activated protein kinase (AMPK) inhibitor, NG-nitro-L-arginine methyl ester, a nitric oxide (NO) synthesis inhibitor and naloxone, an opioid receptor antagonist reversed the effects of phlorizin. In conclusions, phlorizin improved visceral hypersensitivity and colonic hyperpermeability in IBS models. These effects may result from inhibition of SGLT2, and were mediated via AMPK, NO and opioid pathways. Phlorizin may be effective for the treatment of IBS. |
|
言語 |
en |
| 出版タイプ |
|
|
出版タイプ |
AM |
33957565.pdf (1.9 MB)
