Visner G A, Chesrown S E, Monnier J, Ryan U S, Nick H S
Department of Pediatrics, University of Florida, Gainesville 32610.
Biochem Biophys Res Commun. 1992 Oct 15;188(1):453-62. doi: 10.1016/0006-291x(92)92406-n.
IL-1 and TNF are important mediators in the inflammatory response, and have been associated with endothelial cell damage in the lung. TNF and IL-1 cell-mediated injury has been proposed to occur through an increase in intracellular oxygen free radical production. However, these cytokines have also been shown to protect the lung from hyperoxia-mediated oxidant injury. In this paper we evaluated the response of the antioxidant enzymes, MnSOD and Cu/ZnSOD to IL-1, TNF, and LPS in both rat pulmonary artery and microvascular endothelial cells. These mediators produced an increase in MnSOD but not Cu/ZnSOD expression in both rat pulmonary endothelial cells. An additive effect was observed with co-treatment by the cytokines with LPS. The MnSOD mRNA induction is dependent upon a transcriptional event, but did not require de novo protein synthesis.
白细胞介素-1（IL-1）和肿瘤坏死因子（TNF）是炎症反应中的重要介质，且与肺部内皮细胞损伤有关。有人提出TNF和IL-1细胞介导的损伤是通过细胞内氧自由基生成增加而发生的。然而，这些细胞因子也已被证明可保护肺部免受高氧介导的氧化损伤。在本文中，我们评估了抗氧化酶锰超氧化物歧化酶（MnSOD）和铜/锌超氧化物歧化酶（Cu/ZnSOD）在大鼠肺动脉和微血管内皮细胞中对IL-1、TNF和脂多糖（LPS）的反应。这些介质使大鼠肺内皮细胞中MnSOD表达增加，但未使Cu/ZnSOD表达增加。细胞因子与LPS联合处理时观察到了相加效应。MnSOD mRNA的诱导依赖于转录事件，但不需要从头合成蛋白质。
