一氧化氮在内皮细胞损伤中的作用及其受糖皮质激素的抑制作用。
The role of nitric oxide in endothelial cell damage and its inhibition by glucocorticoids.
作者信息
Palmer R M, Bridge L, Foxwell N A, Moncada S
机构信息
Wellcome Research Laboratories, Beckenham, Kent.
出版信息
Br J Pharmacol. 1992 Jan;105(1):11-2. doi: 10.1111/j.1476-5381.1992.tb14202.x.
Abstract
Incubation of vascular endothelial cells with S.typhosa endotoxin and interferon-gamma caused a time- and concentration-dependent reduction in the viability of the cells. The cytotoxic effect was inhibited in a concentration-dependent manner by NG-monomethyl-L-arginine, an inhibitor of nitric oxide (NO) synthesis, and by the glucocorticoids dexamethasone and hydrocortisone, two inhibitors of the induction of NO synthase. These findings indicate that in these cells the cytotoxic effect of endotoxin is mediated by the NO synthesized by an inducible NO synthase. This induction of NO synthase in vascular endothelial cells may represent a mechanism of local endothelial damage during endotoxin shock and other immunologically based conditions.
摘要
用伤寒沙门氏菌内毒素和γ干扰素培养血管内皮细胞，会导致细胞活力呈时间和浓度依赖性降低。一氧化氮（NO）合成抑制剂NG-单甲基-L-精氨酸以及两种诱导型NO合酶诱导抑制剂——糖皮质激素地塞米松和氢化可的松，以浓度依赖性方式抑制了细胞毒性作用。这些发现表明，在这些细胞中，内毒素的细胞毒性作用是由诱导型NO合酶合成的NO介导的。血管内皮细胞中这种诱导型NO合酶的诱导可能代表了内毒素休克和其他基于免疫的病症期间局部内皮损伤的一种机制。
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Glucocorticoids inhibit the expression of an inducible, but not the constitutive, nitric oxide synthase in vascular endothelial cells.糖皮质激素抑制血管内皮细胞中诱导型而非组成型一氧化氮合酶的表达。
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