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首页> 外文期刊>Vascular pharmacology >Sildenafil induces angiogenic response in human coronary arteriolar endothelial cells through the expression of thioredoxin, hemeoxygenase and vascular endothelial growth factor.
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Sildenafil induces angiogenic response in human coronary arteriolar endothelial cells through the expression of thioredoxin, hemeoxygenase and vascular endothelial growth factor.

机译:西地那非通过硫氧还蛋白,血氧合酶和血管内皮生长因子的表达诱导人冠状动脉内皮细胞的血管生成反应。

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摘要

This study was undertaken to investigate the effect of phosphodiesterase-5 (PDE5) inhibitor, sildenafil, on angiogenic response in human coronary arteriolar endothelial cells (HCAEC). The cells exposed to sildenafil (1-20 microM) demonstrated significantly accelerated tubular morphogenesis with the induction of thioredoxin-1 (Trx-1), hemeoxygenase-1 (HO-1) and VEGF. Sildenafil induced VEGF and angiopoietin specific receptors such as KDR, Tie-1 and Tie-2. This angiogenic response was repressed by tinprotoporphyrin IX (SnPP), an inhibitor of HO-1 enzyme activity. Sildenafil below 1 muM has no angiogenic effect as evidenced by reduced tuborogenesis. Sildenafil along with SnPP inhibited both VEGF and Angiopoietin-1 (Ang-1) protein expression. Therefore our results demonstrated for the first time that sildenafil is a very potent pro-angiogenic factor.
机译:进行这项研究以研究磷酸二酯酶5(PDE5)抑制剂西地那非对人冠状动脉内皮细胞(HCAEC)的血管生成反应的影响。暴露于西地那非(1-20 microM)的细胞通过硫氧还蛋白1(Trx-1),血红素加氧酶1(HO-1)和VEGF的诱导表现出显着加速的肾小管形态发生。西地那非诱导VEGF和血管生成素特异性受体,例如KDR,Tie-1和Tie-2。这种血管生成反应被HO-1酶活性抑制剂锡原卟啉IX(SnPP)抑制。低于1μM的西地那非没有血管生成作用,如降低的微管生成所证明。西地那非与SnPP一起抑制VEGF和血管生成素1(Ang-1)蛋白的表达。因此,我们的结果首次证明西地那非是一种非常有效的促血管生成因子。

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