精氨酸酶
一氧化氮合酶
过氧亚硝酸盐
一氧化氮
炎症
医学
发病机制
伤口愈合
病理
下肢静脉性溃疡
血管组织
内科学
化学
免疫学
精氨酸
生物化学
酶
生物
外科
氨基酸
超氧化物
植物
作者
Seham A. Abd‐El‐Aleem,Mark W. J. Ferguson,Ian Appleton,Sadeo Kairsingh,Edward B. Jude,Kelly Jones,Charles McCollum,Grenham W. Ireland
标识
DOI:10.1002/1096-9896(2000)9999:9999<::aid-path654>3.0.co;2-s
摘要
Chronic venous ulcers, an example of abnormal wound healing, show chronic inflammation with defective matrix deposition which together with the underlying vascular pathology, result in delayed healing. L-arginine is known to be metabolized by one of two pathways: nitric oxide synthase (NOS), producing nitric oxide (NO), or arginase, producing ornithine. NO is involved in many pathological conditions including vascular and inflammatory disorders. This study therefore investigated the distribution, level and activity of NOS and arginase in chronic venous ulcers in comparison with normal skin, using immunocytochemistry, western blotting, and enzyme assays. The results demonstrated an increased distribution of both NOS and arginase in chronic venous ulcer tissue compared with normal skin, with inflammatory cells and vascular endothelial cells as the main sources. These data were confirmed by western blot analysis, which showed increased levels of both enzymes in chronic venous ulcers. Moreover, there was significantly increased activity of both total NOS (p<0.04) and inducible NOS (p<0.05) in chronic venous ulcer tissue compared with normal skin, and significantly increased activity of arginase (p<0.01) in chronic venous ulcer tissue in comparison with normal skin. NO is known to combine with hydroxyl free radicals forming peroxynitrite, a potent free radical which causes tissue destruction. NO overexpression in chronic venous ulcers may be involved directly or indirectly (through production of peroxynitrite) in the pathogenesis and delayed healing of chronic venous ulcers, through its effects on vasculature, inflammation, and collagen deposition. Arginase is known to enhance matrix deposition. Thus, increased levels of arginase in chronic venous ulcers could contribute to the pathogenesis of lipodermatosclerosis associated with chronic venous insufficiency, predisposing to the formation of chronic venous ulcers and also to matrix cuff formation around blood vessels. Copyright © 2000 John Wiley & Sons, Ltd.
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