| アイテムタイプ |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2025-11-27 |
| タイトル |
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タイトル |
α7 nicotinic acetylcholine receptor agonist attenuates lipopolysaccharide-induced acute kidney injury in mice by reducing CCL2 expression in macrophages |
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言語 |
en |
| 言語 |
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言語 |
eng |
| 資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
| 著者 |
Matsuo, Sayumi
Uni, Rie
Wu, Chia-Hsien
Nakamura, Yasuna
Umene, Ryusuke
Surattichaiyakul, Bongkod
Nangaku, Masaomi
Inagi, Reiko
Nishino, Tomoya
Inoue, Tsuyoshi
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| 抄録 |
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内容記述タイプ |
Abstract |
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内容記述 |
Sepsis-induced acute kidney injury (AKI) is associated with a high mortality rate and presents a significant clinical challenge. However, effective treatment measures have not yet been established. The cholinergic anti-inflammatory pathway (CAP), a neural mechanism that regulates immune responses, has been reported to mitigate kidney injury. Although numerous studies have demonstrated the benefits of CAP activation prior to injury, its therapeutic potential after the onset of injury remains insufficiently explored. Therefore, this study aimed to evaluate the renoprotective effects of CAP activation after the onset of lipopolysaccharide (LPS)-induced AKI. LPS (5 mg/kg) was administered to C57BL/6 wild-type mice to induce AKI. Subsequently, GTS-21 (10 mg/kg), a selective α7 nicotinic acetylcholine receptor agonist, was administered to assess its anti-inflammatory and renoprotective effects. In RAW 264.7 and U937-derived macrophages, LPS-induced inflammation was treated with GTS-21, and its effects were evaluated. RNA sequencing was performed to elucidate the underlying molecular mechanisms. Even after the onset of LPS-induced AKI, the administration of GTS-21 demonstrated anti-inflammatory and renoprotective effects. In macrophages, the LPS-induced increase in TNF-α was suppressed by GTS-21 (50 μM) administration. Furthermore, CCL2 expression in macrophages might be involved in mediating these effects. |
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言語 |
en |
| 書誌情報 |
en : Scientific Reports
巻 15,
号 1,
p. art. no. 40005,
発行日 2025-11-14
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| 出版者 |
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出版者 |
Springer Nature |
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言語 |
en |
| ISSN |
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収録物識別子タイプ |
EISSN |
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収録物識別子 |
2045-2322 |
| DOI |
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関連タイプ |
isIdenticalTo |
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識別子タイプ |
DOI |
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関連識別子 |
https://doi.org/10.1038/s41598-025-23583-x |
| 権利 |
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権利情報 |
This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/. © The Author(s) 2025 |
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言語 |
en |
| 著者版フラグ |
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出版タイプ |
VoR |
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出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| 引用 |
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内容記述タイプ |
Other |
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内容記述 |
Scientific Reports, 15(1), art. no. 40005; 2025 |
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言語 |
en |
SR15_40005.pdf (2.5 MB)
