地塞米松与大脑中一氧化氮合酶基因的表达
Dexamethasone and nitric oxide synthase gene expression in brain.
作者信息
Suzuki E, Shintani F, Nakaki T, Nagata K, Yamazoe Y, Fujita N, Asai M, Kanba S
机构信息
Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.
出版信息
J Psychiatry Neurosci. 1997 Mar;22(2):105-10.
Systemic administration of lipopolysaccharide (LPS), which causes endotoxemia and systemic inflammation, has been reported to induce expression of the gene for type II inducible nitric oxide synthase (iNOS) in peripheral organs. This study was carried out to examine whether intraperitoneally injected LPS elicits the expression of iNOS messenger ribonucleic acid (mRNA) in the rat brain. We also investigated whether intraperitoneal treatment with dexamethasone (DEX) prevents this induction. To determine levels of iNOS mRNA, a quantitative reverse transcription-polymerase chain reaction (RT-PCR) method was employed. Treatment with LPS induced the expression of iNOS mRNA in various brain regions, accounting for approximately 1 x 10(5) to 4 x 10(5) molecules per micrograms of poly A+ RNA, and these inductions were markedly suppressed by DEX. The results suggest that, during systemic inflammation, iNOS mRNA induction occurs in brain through a DEX-sensitive mechanism.
据报道，全身给予脂多糖（LPS）可导致内毒素血症和全身炎症，进而诱导外周器官中II型诱导型一氧化氮合酶（iNOS）基因的表达。本研究旨在检测腹腔注射LPS是否会引发大鼠脑中iNOS信使核糖核酸（mRNA）的表达。我们还研究了地塞米松（DEX）腹腔注射治疗是否能阻止这种诱导。为了测定iNOS mRNA的水平，采用了定量逆转录-聚合酶链反应（RT-PCR）方法。LPS处理诱导了各个脑区iNOS mRNA的表达，每微克聚腺苷酸加（poly A+）RNA中约有1×10⁵至4×10⁵个分子，而DEX可显著抑制这些诱导。结果表明，在全身炎症期间，iNOS mRNA的诱导通过DEX敏感机制在脑中发生。
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