Testosterone inhibits expression of inducible nitric oxide synthase in murine macrophages
Testosterone inhibits expression of inducible nitric oxide synthase in murine macrophages
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DOI：
10.1016/s0024-3205(00)00953-x
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发表时间：
2000-12-15
期刊：
影响因子：
6.1
通讯作者：
Spieckermann, PG
中科院分区：
文献类型：
--
作者：
Friedl, R;Brunner, M;Spieckermann, PG
我们研究了睾丸酮，男性主要的性类固醇激素，对小鼠巨噬细胞诱导型一氧化氮合成的影响。孵育细菌刺激的小鼠巨噬细胞（RAW 264.7细胞）。脂多糖（2 μ g/ml）与增加量的睾酮（0.1-40 μ M）显示出诱导型一氧化氮合成的剂量依赖性抑制。诱导型一氧化氮合酶蛋白的表达减少，在剂量依赖性的方式揭示了免疫印迹细胞孵育时，增加睾酮的量。这与竞争性半定量PCR测定的iNOS mRNA水平下降有关。由于一氧化氮在免疫防御和动脉粥样硬化预防中起重要作用，睾酮诱导的iNOS抑制可导致感染风险升高以及动脉粥样硬化病变的发展。(C)2000 Elsevier Science Inc. All rights reserved.
We investigated the effect of testosterone, the main sexual steroid hormone in men, upon inducible nitric oxide synthesis in murine macrophages. Incubation of murine macrophages (RAW 264.7 cells) stimulated by bacterial. lipopolysaccharide (2 mug/ml) with increasing amounts of testosterone (0.1-40 muM) showed a dose dependent inhibition of inducible nitric oxide synthesis. Inducible nitric oxide synthase protein expression was reduced in a dose dependent manner as revealed by immunoblotting when cells were incubated with increasing amounts of testosterone. This was associated with a decline in iNOS mRNA-levels as determined by competitive semiquantitative PCR. As nitric oxide plays an important role in immune defense and atherosclerosis prevention, testosterone-induced iNOS inhibition could lead to an elevated risk of infection as well as to the development of atherosclerotic lesions. (C) 2000 Elsevier Science Inc. All rights reserved.