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Activation of the α7nAChR by GTS-21 mitigates septic tubular cell injury and modulates macrophage infiltration
http://hdl.handle.net/10069/0002003427
http://hdl.handle.net/10069/000200342731cab10b-ab50-4046-be0e-26f5c7b14d9f
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
ISYK1723_Yang.pdf (10.6 MB)
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| アイテムタイプ | 学位論文 / Thesis or Dissertation(1) | |||||||
|---|---|---|---|---|---|---|---|---|
| 公開日 | 2025-11-18 | |||||||
| タイトル | ||||||||
| タイトル | Activation of the α7nAChR by GTS-21 mitigates septic tubular cell injury and modulates macrophage infiltration | |||||||
| 言語 | en | |||||||
| 言語 | ||||||||
| 言語 | eng | |||||||
| キーワード | ||||||||
| 言語 | en | |||||||
| 主題Scheme | Other | |||||||
| 主題 | Acute kidney injury | |||||||
| キーワード | ||||||||
| 言語 | en | |||||||
| 主題Scheme | Other | |||||||
| 主題 | α7nAChR | |||||||
| キーワード | ||||||||
| 言語 | en | |||||||
| 主題Scheme | Other | |||||||
| 主題 | Cholinergic anti-inflammatory pathway | |||||||
| キーワード | ||||||||
| 言語 | en | |||||||
| 主題Scheme | Other | |||||||
| 主題 | Macrophage | |||||||
| 資源タイプ | ||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_db06 | |||||||
| 資源タイプ | doctoral thesis | |||||||
| 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 |
楊, 傲冰
× 楊, 傲冰
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| 著者別名 | ||||||||
| 姓名 | Yang, Aobing | |||||||
| 言語 | en | |||||||
| 抄録 | ||||||||
| 内容記述タイプ | Abstract | |||||||
| 内容記述 | The most common and serious complication among hospitalized and critically ill patients is sepsis-associated acute kidney damage (S-AKI), which raises the risk of comorbidities and is linked to a high mortality rate. Cholinergic anti-inflammatory pathway (CAP), an anti-inflammatory pathway mediated by the vagus nerve, acetylcholine, and α7 nicotinic acetylcholine receptors (α7nAChRs), offers new perspectives for the treatment of S-AKI. In this study, we investigated the role of CAP and α7nAChR in kidney injury by employing an LPS-induced septic kidney injury mouse model and GTS-21 intervention. C57BL/6 mice were injected with LPS, with or without GTS-21, in different subgroups. Kidney function was assessed by plasma creatinine, histology, and markers of kidney injury 24 h after intervention. The results demonstrated that GTS-21 could inhibit the systemic inflammatory response and directly protect the tubular cell injury from LPS. To explore the novel gene involved in this response, RNA sequencing of the renal proximal tubular epithelial cell (HK-2), pretreated with LPS and GTS-21, was conducted. The results indicate that GTS-21 administration reduces LPS-induced cytokines and chemokines secretion by HK-2, including CCL20, a potent chemokine attracting monocytes/macrophages. Furthermore, a macrophage transmigration assay revealed that GTS-21 inhibits macrophage transmigration by downregulating the expression of CCL20 in HK-2 cells. In conclusion, GTS-21, as an α7nAChR agonist, emerges as a noteworthy and versatile treatment for S-AKI. Its dual function of directly protecting renal tubular cells and regulating inflammatory responses represents a major advancement in the treatment of sepsis-induced AKI. This finding might pave the way for novel approaches to improving patient outcomes and reducing death rates in sepsis-related complications. | |||||||
| 言語 | en | |||||||
| 内容記述 | ||||||||
| 内容記述タイプ | Other | |||||||
| 内容記述 | 長崎大学学位論文 学位記番号:博(医歯薬)甲第1723号 学位授与年月日:令和7年9月19日 | |||||||
| 言語 | ja | |||||||
| 内容記述 | ||||||||
| 内容記述タイプ | Other | |||||||
| 内容記述 | Author: Aobing Yang, Chia-Hsien Wu, Sayumi Matsuo, Ryusuke Umene, Yasuna Nakamura, Tsuyoshi Inoue | |||||||
| 言語 | en | |||||||
| 内容記述 | ||||||||
| 内容記述タイプ | Other | |||||||
| 内容記述 | Citation: International Immunopharmacology, 138, art. no. 112555; 2024 | |||||||
| 言語 | en | |||||||
| 書誌情報 |
en : International Immunopharmacology 巻 138, p. art. no. 112555, 発行日 2025-09-19 |
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| ISSN | ||||||||
| 収録物識別子タイプ | ISSN | |||||||
| 収録物識別子 | 1567-5769 | |||||||
| DOI | ||||||||
| 関連タイプ | isIdenticalTo | |||||||
| 識別子タイプ | DOI | |||||||
| 関連識別子 | https://doi.org/10.1016/j.intimp.2024.112555 | |||||||
| 権利 | ||||||||
| 権利情報 | © 2024 Elsevier B.V. All rights are reserved, including those for text and data mining, AI training, and similar technologies. | |||||||
| 言語 | en | |||||||
| 著者版フラグ | ||||||||
| 出版タイプ | VoR | |||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||
| その他のタイトル | ||||||||
| その他のタイトル | GTS-21によるα7nAChRの活性化は、敗血症性尿細管細胞障害を軽減し、マクロファージの浸潤を調節する | |||||||
| 言語 | ja | |||||||
| 出版者 | ||||||||
| 出版者 | Elsevier B.V. | |||||||
| 言語 | en | |||||||
| 関係URI | ||||||||
| 識別子タイプ | HDL | |||||||
| 関連識別子 | http://hdl.handle.net/10069/0002003330 | |||||||
| 学位名 | ||||||||
| 学位名 | 博士(医学) | |||||||
| 言語 | ja | |||||||
| 学位授与機関 | ||||||||
| 学位授与機関識別子Scheme | kakenhi | |||||||
| 学位授与機関識別子 | 17301 | |||||||
| 学位授与機関名 | Nagasaki University (長崎大学) | |||||||
| 学位授与年月日 | ||||||||
| 学位授与年月日 | 2025-09-19 | |||||||
| 学位授与番号 | ||||||||
| 学位授与番号 | 甲医歯薬第1723号 | |||||||
| 学位の種類 | ||||||||
| 言語 | ja | |||||||
| 値 | 課程博士 | |||||||
| 引用 | ||||||||
| 内容記述タイプ | Other | |||||||
| 内容記述 | Nagasaki University (長崎大学), 博士(医学) (2025-09-19) | |||||||
