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首页> 外文期刊>American Journal of Physiology >Tyrosine kinase inhibitors and antioxidants modulate NF-kappaB and NOS-II induction in retinal epithelial cells.
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Tyrosine kinase inhibitors and antioxidants modulate NF-kappaB and NOS-II induction in retinal epithelial cells.

机译：酪氨酸激酶抑制剂和抗氧化剂可调节视网膜上皮细胞中的NF-κB和NOS-II诱导。

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摘要

Bovine retinal pigmented epithelial (RPE) cells express an inducible nitric oxide synthase (NOS-II) after activation with interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS). Experiments were performed to investigate the effects of tyrosine kinase inhibitors (genistein and herbimycin A) and antioxidants [pyrrolidine dithiocarbamate (PDTC) and butyl hydroxyanisol] on NOS-II induction. The LPS-IFN-gamma-induced nitrite release was inhibited in a concentration-dependent manner by these compounds. Analysis by Northern blot showed that this inhibitory effect correlated with a decrease in NOS-II mRNA accumulation. Analysis by electrophoretic mobility shift assay of the activation of the transcription factor nuclear factor-kappaB (NF-kappaB) involved in NOS-II induction demonstrated that LPS alone or combined with IFN-gamma induced NF-kappaB binding. NF-kappaB activation was not changed by the presence of tyrosine kinase inhibitors but was totally prevented by PDTC pretreatment. Immunocytochemistry experiments confirmed the reduction of the nuclear translocation of NF-kappaB only by PDTC. Our results demonstrated the existence in retinal pigmented epithelial cells of different intracellular signaling pathways in NOS-II induction, since tyrosine kinase inhibitors blocked NOS-II mRNA accumulation without inhibiting NF-kappaB activation. Furthermore, the LPS-IFN-gamma-induced NOS-II mRNA accumulation was sensitive to cycloheximide, suggesting that, in addition to NF-kappaB, transcriptional factors that require new protein synthesis are involved in NOS-II induction.
机译：牛视网膜色素上皮细胞（RPE）在被干扰素-γ（IFN-γ）和脂多糖（LPS）激活后表达诱导型一氧化氮合酶（NOS-II）。进行实验以研究酪氨酸激酶抑制剂（染料木黄酮和除草素A）和抗氧化剂[吡咯烷二硫代氨基甲酸酯（PDTC）和丁基羟基茴香醚]对NOS-II诱导的影响。这些化合物以浓度依赖的方式抑制LPS-IFN-γ诱导的亚硝酸盐释放。 Northern印迹分析表明，这种抑制作用与NOS-II mRNA积累的减少有关。通过电泳迁移率变动分析法分析参与NOS-II诱导的转录因子核因子-κB（NF-kappaB）的激活，表明LPS单独或与IFN-γ结合可诱导NF-kappaB结合。酪氨酸激酶抑制剂的存在不会改变NF-κB的活化，但是PDTC预处理可以完全阻止NF-κB的活化。免疫细胞化学实验证实只有PDTC可以减少NF-κB的核转运。我们的研究结果表明，由于酪氨酸激酶抑制剂在不抑制NF-κB活化的情况下阻断了NOS-II mRNA的积累，因此在NOS-II诱导中存在着不同细胞内信号通路的视网膜色素上皮细胞的存在。此外，LPS-IFN-γ诱导的NOS-II mRNA积累对环己酰亚胺敏感，这表明，除了NF-κB外，需要新蛋白质合成的转录因子也参与了NOS-II的诱导。

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