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血红素加氧酶-1在大鼠佐剂性关节炎进展中的潜在作用。

Potential role of heme oxygenase-1 in the progression of rat adjuvant arthritis.

作者信息

Devesa Isabel, Ferrándiz Maria Luisa, Guillén Isabel, Cerdá José Miguel, Alcaraz Maria José

机构信息

Department of Pharmacology, University of Valencia, Valencia, Spain.

出版信息

Lab Invest. 2005 Jan;85(1):34-44. doi: 10.1038/labinvest.3700205.

Abstract

Rat adjuvant arthritis is an experimental model widely used to evaluate etiopathogenetic mechanisms in chronic inflammation. We have examined the participation of heme oxygenase-1 (HO-1) in this experimental arthritis. In this study, an increased nitric oxide (NO) production in the paw preceded the upregulation of HO-1, whereas selective inhibition of inducible NO synthase (iNOS) after the onset of arthritis decreased HO-1 expression, suggesting that the induction of this enzyme may depend on NO produced by iNOS. Therapeutic administration of the HO-1 inhibitor tin protoporphyrin IX was able to control the symptoms of arthritis. This agent significantly decreased leukocyte infiltration, hyperplastic synovitis, erosion of articular cartilage and osteolysis, as well as the production of inflammatory mediators. In this experimental model, HO-1 can be involved in vascular endothelial growth factor production and angiogenesis. These results support a role for HO-1 in mediating the progression of the disease in this model of chronic arthritis.

摘要

大鼠佐剂性关节炎是一种广泛用于评估慢性炎症发病机制的实验模型。我们研究了血红素加氧酶-1(HO-1)在这种实验性关节炎中的作用。在本研究中,爪部一氧化氮(NO)产量增加先于HO-1上调,而关节炎发作后选择性抑制诱导型一氧化氮合酶(iNOS)可降低HO-1表达,提示该酶的诱导可能依赖于iNOS产生的NO。HO-1抑制剂锡原卟啉IX的治疗性给药能够控制关节炎症状。该药物显著减少白细胞浸润、增生性滑膜炎、关节软骨侵蚀和骨质溶解,以及炎症介质的产生。在这个实验模型中,HO-1可能参与血管内皮生长因子的产生和血管生成。这些结果支持HO-1在介导该慢性关节炎模型中疾病进展方面的作用。

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