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Phlorizin attenuates visceral hypersensitivity and colonic hyperpermeability in a rat model of irritable bowel syndrome

https://asahikawa-med.repo.nii.ac.jp/records/2000473
https://asahikawa-med.repo.nii.ac.jp/records/2000473
792114d7-7b33-4b68-8661-b9740638ae23
名前 / ファイル ライセンス アクション
33957565.pdf 33957565.pdf (1.9 MB)
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

× 野津, 司

ja 野津, 司

ja-Kana ノヅ, ツカサ

en Nozu, Tsukasa

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宮岸, 沙織

× 宮岸, 沙織

ja 宮岸, 沙織

ja-Kana ミヤギシ, サオリ

en Miyagishi, Saori

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石王, 応知

× 石王, 応知

ja 石王, 応知

ja-Kana イシオウ, マサトモ

en Ishioh, Masatomo

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高草木, 薫

× 高草木, 薫

ja 高草木, 薫

ja-Kana タカクサキ, カオル

en Takakusaki, Kaoru

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奥村, 利勝

× 奥村, 利勝

ja 奥村, 利勝

ja-Kana オクムラ, トシカツ

en Okumura, Toshikatsu

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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
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