Involvement of nitric oxide in a rat model of carrageenin-induced pleurisy.

Involvement of nitric oxide in a rat model of carrageenin-induced pleurisy.
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DOI:
10.1155/2010/682879
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发表时间:
2010
影响因子:
4.6
通讯作者:
Takagi K
Takagi K
中科院分区:
医学3区
文献类型:
--
作者:
Iwata M;Suzuki S;Asai Y;Inoue T;Takagi K

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一些证据表明,一氧化氮(NO)有助于炎症,而另一些证据则支持相反的结论。为了阐明NO在炎症中的作用,我们研究了用NO供体(NOC-18)、NO形成底物(L-精氨酸)和/或NO合成酶抑制剂(S-(2-氨基乙基)异硫脲或NG-硝基-L-精氨酸)处理的角叉菜胶致大鼠胸膜炎。我们评估了炎症细胞迁移、亚硝酸盐/硝酸根比值、脂质过氧化和促炎介质。NOC-18和L-精氨酸减少炎症细胞的迁移和水肿,降低氧化应激,并使抗氧化酶活性正常化。NO合酶抑制剂增加渗出物的形成和炎症细胞的数量,促进氧化应激,通过维持高O2−而诱导氧化/抗氧化失衡,并促进促炎介质的产生。L-精氨酸和NOC-18逆转了NO合成酶抑制剂的促炎作用,可能是通过减少内皮细胞上黏附分子的表达而实现的。因此,我们的结果表明,NO参与了钝化而不是增强炎症反应。
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 O2 −, 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.
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