Erdogan Ali, Luedders Doerte Wiebke, Muenz Benedikt Manuel, Schaefer Christian Alexander, Tillmanns Harald, Wiecha Johannes, Kuhlmann Christoph Ruediger Wolfram
Department of Cardiology and Angiology, Justus-Liebig University of Giessen;
Int J Biomed Sci. 2007 Jun;3(2):93-6.
The proliferation of endothelial cells plays a crucial role in the development of intraplaque angiogenesis (IPA). IPA is a major source of intraplaque hemorrhage and therefore contributes to the destabilization of atherosclerotic plaques. Therefore, the aim of the present study was to examine, whether sildenafil inhibits endothelial cell growth. The proliferation of human endothelial cells derived from umbilical cord veins (HUVEC) was examined on DNA level by measurements of ((3)H)-thymidine incorporation. Cell viability was analyzed using trypan blue staining. The proliferation of cultured human endothelial cells was significantly decreased by 1 μmol/l (-48.4%) and 10 μmol/l (-89.6%) sildenafil (n=10, p<0.05). This was not a cytotoxic effect, because cell viability was only reduced at sildenafil concentrations of 50 μmol/l or greater. In addition sildenafil significantly reduced endothelial proliferation induced by bFGF (n=10, p<0.05). The presented results demonstrate an antiangiogenic effect of sildenafil that might be useful in the prevention of atherosclerotic plaque vascularization.
内皮细胞的增殖在斑块内血管生成（IPA）的发展中起着关键作用。IPA是斑块内出血的主要来源，因此会导致动脉粥样硬化斑块的不稳定。因此，本研究的目的是检验西地那非是否抑制内皮细胞生长。通过测量（³H）-胸腺嘧啶核苷掺入量，在DNA水平上检测源自人脐静脉的内皮细胞（HUVEC）的增殖。使用台盼蓝染色分析细胞活力。1 μmol/l（-48.4%）和10 μmol/l（-89.6%）的西地那非显著降低了培养的人内皮细胞的增殖（n = 10，p < 0.05）。这不是细胞毒性作用，因为只有在西地那非浓度为50 μmol/l或更高时细胞活力才会降低。此外，西地那非显著降低了由碱性成纤维细胞生长因子（bFGF）诱导的内皮细胞增殖（n = 10，p < 0.05）。所呈现的结果表明西地那非具有抗血管生成作用，这可能对预防动脉粥样硬化斑块血管化有用。
