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Decreased death receptor pathway of apoptotic signaling in the septic mouse gut: effect of nutritional support
https://doi.org/10.15100/0002001136
https://doi.org/10.15100/00020011365553b596-3573-4ec6-873c-6a06ff7b7fff
名前 / ファイル | ライセンス | アクション |
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Item type | 紀要論文 / departmental bulletin paper(1) | |||||||
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公開日 | 2024-06-20 | |||||||
タイトル | ||||||||
タイトル | Decreased death receptor pathway of apoptotic signaling in the septic mouse gut: effect of nutritional support | |||||||
言語 | en | |||||||
作成者 |
Futatsugi, Motonori
× Futatsugi, Motonori
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言語 | ||||||||
言語 | eng | |||||||
キーワード | ||||||||
主題 | sepsis, nutritional support, death receptor | |||||||
内容記述 | ||||||||
内容記述タイプ | Abstract | |||||||
内容記述 | Background: Sepsis is a systemic inflammatory response syndrome (SIRS) caused by infection. Sepsis remains a cause of death in patients in intensive care. In sepsis, death receptors such as tumor necrosis factor receptor 1 (TNF-R1), Fas, and caspase-3 are related to sepsis-induced apoptosis. Conversely, the nutritional support including enteral nutrition (EN) is considered an effective therapy in the intensive care unit. In the digestive tract, the detailed mechanisms of these death receptors and caspase-3 remain unknown in septic status. Methods: We examined the expression of TNF-R1, Fas, and activated caspase-3 and compared the effect of nutritional support with EN in the digestive tract of septic mice. Polymicrobial sepsis was induced by cecal ligation and puncture(CLP) in CD1/ICR mice. We investigated TNF-R1, Fas, and caspase-3 activation in the mouse digestive tract and compared different feed therapies including EN. Result: In this study, we observed that the expression of TNF-R1, Fas, and cleaved caspase-3 was elevated in the duodenum, jejunum, and ileum of CLP-induced septic mice. In the ileum of CLP-induced septic mice with EN, the expression of death receptors (TNF-R1 and Fas) and cleaved caspase-3 was downregulated. Conclusions: In the digestive tract, our results suggest that nutritional support including EN can be an effective therapy for sepsis-induced apoptosis. |
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言語 | en | |||||||
出版者 | ||||||||
出版者 | The Kindai University Medical Association | |||||||
言語 | en | |||||||
資源タイプ | ||||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||
資源タイプ | departmental bulletin paper | |||||||
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出版タイプ | AM | |||||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||||
ID登録 | ||||||||
ID登録 | 10.15100/0002001136 | |||||||
ID登録タイプ | JaLC | |||||||
収録物識別子 | ||||||||
収録物識別子タイプ | PISSN | |||||||
収録物識別子 | 03866092 | |||||||
収録物識別子 | ||||||||
収録物識別子タイプ | EISSN | |||||||
収録物識別子 | 24327166 | |||||||
書誌情報 |
en : ACTA MEDICA KINDAI UNIVERSITY 巻 49, 号 1, p. 7-13, 発行日 2024-06 |