WEKO3
アイテム
Involvement of Nitric Oxide in a Rat Model of Carrageenin-Induced Pleurisy
http://hdl.handle.net/2237/22970
http://hdl.handle.net/2237/229700581972c-272c-430b-829d-fd898a45a0bc
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
682879.pdf (1.5 MB)
|
|
| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2015-09-02 | |||||
| タイトル | ||||||
| タイトル | Involvement of Nitric Oxide in a Rat Model of Carrageenin-Induced Pleurisy | |||||
| 言語 | en | |||||
| 著者 |
Iwata, Masahiro
× Iwata, Masahiro× Suzuki, Shigeyuki× Asai, Yuji× Inoue, Takayuki× Takagi, Kenji |
|||||
| 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 | |||||
| 権利 | ||||||
| 言語 | en | |||||
| 権利情報 | Copyright © 2010 Masahiro Iwata et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Some evidence indicates that nitric oxide (NO) contributes to inflammation, while other evidence supports the opposite conclusion. To clarify the role of NO in inflammation, we studied carrageenin-induced pleurisy in rats treated with an NO donor (NOC-18), a substrate for NO formation (L-arginine), and/or an NO synthase inhibitor (S-(2-aminoethyl) isothiourea or -nitro-L-arginine). We assessed inflammatory cell migration, nitrite/nitrate values, lipid peroxidation and pro-inflammatory mediators. NOC-18 and L-arginine reduced the migration of inflammatory cells and edema, lowered oxidative stress, and normalized antioxidant enzyme activities. NO synthase inhibitors increased the exudate formation and inflammatory cell number, contributed to oxidative stress, induced an oxidant/antioxidant imbalance by maintaining high , and enhanced the production of pro-inflammatory mediators. L-arginine and NOC-18 reversed the proinflammatory effects of NO synthase inhibitors, perhaps by reducing the expression of adhesion molecules on endothelial cells. Thus, our results indicate that NO is involved in blunting—not enhancing—the inflammatory response. | |||||
| 言語 | en | |||||
| 出版者 | ||||||
| 出版者 | Hindawi | |||||
| 言語 | en | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプresource | http://purl.org/coar/resource_type/c_6501 | |||||
| タイプ | journal article | |||||
| 出版タイプ | ||||||
| 出版タイプ | VoR | |||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
| DOI | ||||||
| 関連タイプ | isVersionOf | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | https://doi.org/10.1155/2010/682879 | |||||
| ISSN | ||||||
| 収録物識別子タイプ | PISSN | |||||
| 収録物識別子 | 0962-9351 | |||||
| 書誌情報 |
en : Mediators of Inflammation 巻 2010, p. 682879-682879, 発行日 2010 |
|||||
| 著者版フラグ | ||||||
| 値 | publisher | |||||
| URI | ||||||
| 識別子 | http://dx.doi.org/10.1155/2010/682879 | |||||
| 識別子タイプ | DOI | |||||
| URI | ||||||
| 識別子 | http://hdl.handle.net/2237/22970 | |||||
| 識別子タイプ | HDL | |||||
