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首页> 外文期刊>Journal of Cellular Physiology >Effect of antioxidants on lipopolysaccharide-stimulated induction of mangano superoxide dismutase mRNA in bovine pulmonary artery endothelial cells.
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Effect of antioxidants on lipopolysaccharide-stimulated induction of mangano superoxide dismutase mRNA in bovine pulmonary artery endothelial cells.

机译：抗氧化剂对lipopolysaccharide-stimulated感应的曼格诺超氧化物歧化酶mRNA在牛肺动脉内皮细胞。

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摘要

Generation of reactive oxygen species (ROS) is a common event in the pathogenesis of acute lung injury. Endothelial cells may be both a target and a source of the ROS. Exposure of bovine pulmonary endothelial cells (BPAEC) to lipopolysaccharide (LPS) has been shown to result in intracellular generation of both ROS and the antioxidant enzyme, mangano superoxide dismutase (MnSOD). The present study investigates whether alterations in intracellular oxidant state affect LPS-stimulated cytotoxicity and induction of MnSOD mRNA. BPAEC were pretreated with either the free radical scavenger, dimethylsulfoxide (DMSO), the xanthine oxidase inhibitor, allopurinol, or N-acetylcysteine (a cysteine derivate capable of increasing glutathione stores) prior to exposure to LPS (0.1 microgram/ml) for either 4, 8 or 18 hours. We found that pretreatment of BPAEC with DMSO blocked both LPS-induced cytotoxicity and induction of the MnSOD gene. Nuclear run-off experiments demonstrated that LPS-stimulated induction of the MnSODmRNA occurred at the transcriptional level and that DMSO blocked this event. Pretreatment with allopurinol also prevented the cytotoxicity associated with LPS but, in contrast to DMSO, did not alter induction of MnSOD mRNA. N-acetylcysteine did not affect the LPS-stimulated cytotoxicity but resulted in an early and transient reduction in induction of the MnSOD gene. We conclude that LPS stimulates generation of intracellular ROS that regulate induction of the MnSOD gene at the transcriptional level further, we conclude that LPS-stimulated cytotoxicity involves both the xanthine oxidase pathway and perhaps intracellular generation of hydroxyl radicals. The difference in the protective effect between DMSO, NAC and allopurinol suggest that upregulation of the MnSOD gene does not contribute to LPS-induced cytotoxicity.
机译：代的活性氧(ROS)公共事件在急性肺的发病机制受伤。和活性氧的来源。肺动脉内皮细胞(BPAEC)脂多糖(LPS)已被证明的结果在细胞内ROS和的一代抗氧化酶,曼格诺超氧化物歧化酶(MnSOD)。改变细胞内氧化剂状态影响LPS-stimulated细胞毒性和诱导MnSOD mRNA。自由基清除剂,二甲亚砜(DMSO),黄嘌呤氧化酶抑制剂、别嘌呤醇或防治(半胱氨酸衍生物的能力在曝光之前增加谷胱甘肽的商店)有限合伙人(0.1微克/毫升)4、8、18个小时。LPS-induced细胞毒性和DMSO阻塞感应的MnSOD基因。实验表明,LPS-stimulated归纳MnSODmRNA发生的转录水平和DMSO封锁了这个事件。阻止了细胞毒性与有限合伙人但是,在DMSO溶液相比,没有改变感应MnSOD信使rna。LPS-stimulated细胞毒性而导致减少早期和瞬态感应的MnSOD基因。代的细胞内ROS调节归纳MnSOD基因的转录水平进一步,我们得出这样的结论:LPS-stimulated细胞毒性包括两个黄嘌呤氧化酶途径和可能细胞内生成羟基自由基。的差异之间的保护作用DMSO,南汽和别嘌呤醇显示upregulation MnSOD基因的没有导致LPS-induced细胞毒性。

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