Involvement of Nitric Oxide in a Rat Model of Carrageenin-Induced Pleurisy
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),...
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| Format: | Article |
| Language: | English |
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Wiley
2010-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2010/682879 |
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| _version_ | 1832561770741366784 |
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| author | Masahiro Iwata Shigeyuki Suzuki Yuji Asai Takayuki Inoue Kenji Takagi |
| author_facet | Masahiro Iwata Shigeyuki Suzuki Yuji Asai Takayuki Inoue Kenji Takagi |
| author_sort | Masahiro Iwata |
| collection | DOAJ |
| description | 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 NG-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 O−2, 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. |
| format | Article |
| id | doaj-art-660802eabbda4a2587f3948be048bd6a |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2010-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-660802eabbda4a2587f3948be048bd6a2025-02-03T01:24:14ZengWileyMediators of Inflammation0962-93511466-18612010-01-01201010.1155/2010/682879682879Involvement of Nitric Oxide in a Rat Model of Carrageenin-Induced PleurisyMasahiro Iwata0Shigeyuki Suzuki1Yuji Asai2Takayuki Inoue3Kenji Takagi4Department of Rehabilitation, Faculty of Health Sciences, Nihon Fukushi University, 26-2 Higashihaemi-cho, Handa 475-0012, JapanDepartment of Physical Therapy, Nagoya University School of Health Sciences, 1-1-20 Daikominami, Higashi-ku, Nagoya 461-8673, JapanDepartment of Rehabilitation, Faculty of Health Sciences, Nihon Fukushi University, 26-2 Higashihaemi-cho, Handa 475-0012, JapanDepartment of Rehabilitation, Nagoya University Hospital, 1-1-20 Daikominami, Higashi-ku, Nagoya 461-8673, JapanProgram in Radiological and Medical Laboratory Sciences, Nagoya University Graduate School of Medicine, 1-1-20 Daikominami, Higashi-ku, Nagoya 461-8673, JapanSome 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 NG-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 O−2, 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.http://dx.doi.org/10.1155/2010/682879 |
| spellingShingle | Masahiro Iwata Shigeyuki Suzuki Yuji Asai Takayuki Inoue Kenji Takagi Involvement of Nitric Oxide in a Rat Model of Carrageenin-Induced Pleurisy Mediators of Inflammation |
| title | Involvement of Nitric Oxide in a Rat Model of Carrageenin-Induced Pleurisy |
| title_full | Involvement of Nitric Oxide in a Rat Model of Carrageenin-Induced Pleurisy |
| title_fullStr | Involvement of Nitric Oxide in a Rat Model of Carrageenin-Induced Pleurisy |
| title_full_unstemmed | Involvement of Nitric Oxide in a Rat Model of Carrageenin-Induced Pleurisy |
| title_short | Involvement of Nitric Oxide in a Rat Model of Carrageenin-Induced Pleurisy |
| title_sort | involvement of nitric oxide in a rat model of carrageenin induced pleurisy |
| url | http://dx.doi.org/10.1155/2010/682879 |
| work_keys_str_mv | AT masahiroiwata involvementofnitricoxideinaratmodelofcarrageenininducedpleurisy AT shigeyukisuzuki involvementofnitricoxideinaratmodelofcarrageenininducedpleurisy AT yujiasai involvementofnitricoxideinaratmodelofcarrageenininducedpleurisy AT takayukiinoue involvementofnitricoxideinaratmodelofcarrageenininducedpleurisy AT kenjitakagi involvementofnitricoxideinaratmodelofcarrageenininducedpleurisy |