| Item type |
文献 / Documents(1) |
| 公開日 |
2024-10-02 |
| 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 |
| 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 |
journal article |
| item_1722929371688 |
|
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.1371/journal.pone.0086335 |
|
|
言語 |
ja |
|
|
関連名称 |
10.1371/journal.pone.0086335 |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| タイトル |
|
|
タイトル |
Nitrosonifedipine Ameliorates the Progression of Type 2 Diabetic Nephropathy by Exerting Antioxidative Effects |
|
言語 |
en |
| タイトル別表記 |
|
|
その他のタイトル |
Nitrosonifedipine Ameliorates Diabetic Nephropathy |
|
言語 |
en |
| 著者 |
石澤, 啓介
(井澤)石澤, 有紀
Yamano, Noriko
漆原, 真樹
Sakurada, Takumi
今西, 正樹
Fujii, Shoko
Nuno, Asami
宮本, 理人
木平, 孝高
池田, 康将
香美, 祥二
Kobori, Hiroyuki
土屋, 浩一郎
玉置, 俊晃
|
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
Diabetic nephropathy (DN) is the major cause of end-stage renal failure. Oxidative stress is implicated in the pathogenesis of DN. Nitrosonifedipine (NO-NIF) is a weak calcium channel blocker that is converted from nifedipine under light exposure. Recently, we reported that NO-NIF has potential as a novel antioxidant with radical scavenging abilities and has the capacity to treat vascular dysfunction by exerting an endothelial protective effect. In the present study, we extended these findings by evaluating the efficacy of NO-NIF against DN and by clarifying the mechanisms of its antioxidative effect. In a model of type 2 DN (established in KKAy mice), NO-NIF administration reduced albuminuria and proteinuria as well as glomerular expansion without affecting glucose metabolism or systolic blood pressure. NO-NIF also suppressed renal and systemic oxidative stress and decreased the expression of intercellular adhesion molecule (ICAM)-1, a marker of endothelial cell injury, in the glomeruli of the KKAy mice. Similarly, NO-NIF reduced albuminuria, oxidative stress, and ICAM-1 expression in endothelial nitric oxide synthase (eNOS) knockout mice. Moreover, NO-NIF suppressed urinary angiotensinogen (AGT) excretion and intrarenal AGT protein expression in proximal tubular cells in the KKAy mice. On the other hand, hyperglycemia-induced mitochondrial superoxide production was not attenuated by NO-NIF in cultured endothelial cells. These findings suggest that NO-NIF prevents the progression of type 2 DN associated with endothelial dysfunction through selective antioxidative effects. |
|
言語 |
en |
| bibliographic_information |
en : PLOS ONE
巻 9,
号 1,
p. e86335,
発行日 2014-01-28
|
| 収録物ID |
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|
収録物識別子タイプ |
EISSN |
|
収録物識別子 |
19326203 |
| 出版者 |
|
|
出版者 |
PLOS |
|
言語 |
en |
| item_10001_rights_15 |
|
|
言語 |
en |
|
権利情報 |
This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
| item_1723180141928 |
|
|
識別子 |
275165 |
|
識別子タイプ |
URI |
| 言語 |
|
|
言語 |
eng |
pone_9_1_e86335.pdf (1.5 MB)
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