Acta Pharm. 2014 Mar;64(1):131-8. doi: 10.2478/acph-2014-0006.
Diclofenac belongs to non-steroidal anti-inflammatory drugs (NSAIDs) and non-selective COX inhibitors. The aim of this study was to examine the effect of diclofenac on endothelial cell proliferation under the influence of hypoxia or inflammatory conditions. Another goal was to check whether diclofenac modulates the secretion of angiogenic factors such as VEGF and bFGF in human microvascular endothelial cells (HMEC-1) in the presence of CoCl2 or lipopolysaccharide (LPS), which could influence the endothelial cells in an autocrine manner or other cells in a paracrine manner. HMEC-1 cells were treated with 0.1 and 0.3 mmol L-1 diclofenac in the presence of 100 μg mL-1 LPS or 200 μmol L-1 CoCl2. Diclofenac decreased cell viability under hypoxia and inflammatory conditions. The stimulation of bFGF secretion by LPS in microvascular endothelial cells (HMEC-1 cell) was attenuated by diclofenac. Diclofenac increased the secretion of VEGF induced by LPS and hypoxia.
双氯芬酸属于非甾体抗炎药（NSAIDs）和非选择性 COX 抑制剂。本研究旨在研究双氯芬酸在缺氧或炎症条件下对内皮细胞增殖的影响。另一个目的是检查双氯芬酸是否能调节血管生成因子的分泌，如在 CoCl2 或脂多糖（LPS）存在的情况下，血管内皮生长因子（VEGF）和碱性成纤维细胞生长因子（bFGF）在人微血管内皮细胞（HMEC-1）中，这可能以自分泌的方式影响内皮细胞或以旁分泌的方式影响其他细胞。用 0.1 和 0.3mmol L-1 双氯芬酸处理 100μg mL-1 LPS 或 200μmol L-1 CoCl2 存在下的 HMEC-1 细胞。双氯芬酸降低缺氧和炎症条件下细胞活力。双氯芬酸减弱了 LPS 刺激微血管内皮细胞（HMEC-1 细胞）中 bFGF 分泌。双氯芬酸增加了 LPS 和缺氧诱导的 VEGF 分泌。
