首页> 外文期刊>Polish journal of pharmacology >Inhibition of nitric oxide synthase prevents energy failure and oxidative damage evoked in the brain by lipopolysaccharide.
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Inhibition of nitric oxide synthase prevents energy failure and oxidative damage evoked in the brain by lipopolysaccharide.

机译:抑制一氧化氮合酶可防止能量衰竭和脂多糖在大脑中引起的氧化损伤。

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摘要

The inducible nitric oxide synthase (iNOS) plays an important role in endotoxic shock. However,little is known about the involvment of constitutive isoform(s) of NOS (cNOS). The aim of this study was to determine the role of cNOS in the mouse brain after lipopolysaccharide (LPS) injection. Concentrations of nicotinamide adenine dinucleotide (NAD(+)), carbonyl group and thiobarbituric acid reactive substances were determined spectrophotometrically, cNOS mRNA was evaluated by RT-PCR. Our data showed that LPS significantly decreased NAD(+) level, and enhanced protein and lipid oxidation, but had no effect on cNOS mRNA expression. Inhibitors of cNOS protected the cells against alterations evoked by LPS, suggesting involvement of cNOS isoforms in pathology.
机译:诱导型一氧化氮合酶(iNOS)在内毒素休克中起重要作用。然而,关于NOS(cNOS)的组成型同工型的了解很少。这项研究的目的是确定脂多糖(LPS)注射后cNOS在小鼠脑中的作用。分光光度法测定烟酰胺腺嘌呤二核苷酸(NAD(+)),羰基和硫代巴比妥酸反应性物质的浓度,通过RT-PCR评估cNOS mRNA。我们的数据显示LPS显着降低了NAD(+)水平,并增强了蛋白质和脂质的氧化作用,但对cNOS mRNA表达没有影响。 cNOS抑制剂可保护细胞免受LPS引起的改变,提示cNOS同工型参与了病理研究。

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