内皮功能障碍在老鼠adjuvant-induced关节炎:血管过氧化物生产NAD (P) H氧化酶和非耦合内皮一氧化氮合酶。
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Haruna Y,盛田昭夫Y, Komai N,雅达T, Sakuta T,获利,N,福克斯哒,Kashihara N
内皮功能障碍在老鼠adjuvant-induced关节炎:血管过氧化物生产NAD (P) H氧化酶和非耦合内皮一氧化氮合酶。
关节炎感冒。2006年6月,54 (6):1847 - 55。
- PubMed ID
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16729278 (在PubMed]
- 文摘
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摘要目的:探讨内皮功能和血管氧化应激水平鼠adjuvant-induced关节炎(AIA),鉴于越来越多的证据对类风湿性关节炎(RA)之间的关联和加速血管疾病。方法:准备从友邦保险和胸主动脉环控制老鼠。preconstriction由去甲肾上腺素后,常认为乙酰胆碱是确定的。大量4-hydroxy-2-nonenal (HNE)和硝基酪氨酸友邦鼠主动脉被西方墨点法测量。主动脉匀浆的孵化与各种基质superoxide-producing酶和过氧化物生产被fluorogenic评估氧化dihydroethidium ethidium。内皮一氧化氮合酶的表达了(以挪士)在主动脉实时反向transcriptase-polymerase连锁反应和免疫印迹。血清水平的四氢生物蝶呤(BH4),一个关键以挪士代数余子式,通过高效液相色谱法测定。结果:Endothelium-dependent放松友邦主动脉环明显沮丧的老鼠相比,控制老鼠。HNE和硝基酪氨酸的含量增加友邦鼠主动脉,表明活性氧的生产过剩。孵化的友邦鼠主动脉匀浆NADH或精氨酸,以挪士的衬底,导致超氧化物产量显著增加。 Endothelial NOS was highly expressed in AIA rat aortas. Serum levels of BH4 were significantly lower in AIA. Treatment of AIA with BH4 reversed the endothelial dysfunction, suggesting that its deficiency may contribute to the uncoupling of eNOS. CONCLUSION: Vascular dysfunction in RA can be partially modeled in animals. NAD(P)H oxidase and uncoupled eNOS are responsible for the increase in vascular oxidative stress, which is likely to be involved in the endothelial dysfunction in AIA.