Wang Weiwei, Liu Xia, Zhao Jing, Zhao Baoxiang, Zhang Shangli, Miao Junying
Institute of Developmental Biology, School of Life Science, Shandong University, Jinan 250100, China.
Bioorg Med Chem Lett. 2007 Jan 15;17(2):482-5. doi: 10.1016/j.bmcl.2006.10.023. Epub 2006 Oct 12.
To understand the effects of a novel butyrolactone derivative, 3-benzyl-5-((2-nitrophenoxy) methyl)-dihydrofuran-2(3H)-one (3BDO), on the apoptosis of vascular endothelial cells (VECs), we exposed 3BDO (20-60 microg/ml) to VECs deprived of serum and FGF-2 for 24 and 48 h, respectively. The results showed that 3BDO (20-60 microg/ml) increased VEC viability and inhibited VEC apoptosis induced by deprivation of serum and FGF-2 in a very weak dose-dependent manner. During this process, integrin beta4 expression was depressed, but the level of reactive oxygen species (ROS) was not changed. The data suggested that 3BDO (20-60 microg/ml) could inhibit VEC apoptosis and suppress integrin beta4 expression, but it could not depress the ROS level induced by deprivation of serum and FGF-2.
为了解新型丁内酯衍生物3-苄基-5-((2-硝基苯氧基)甲基)-二氢呋喃-2(3H)-酮(3BDO)对血管内皮细胞(VECs)凋亡的影响，我们分别将3BDO(20 - 60μg/ml)作用于血清和碱性成纤维细胞生长因子-2(FGF-2)缺失的VECs 24小时和48小时。结果显示，3BDO(20 - 60μg/ml)可提高VECs活力，并以非常微弱的剂量依赖性方式抑制血清和FGF-2缺失诱导的VECs凋亡。在此过程中，整合素β4表达降低，但活性氧(ROS)水平未发生变化。数据表明，3BDO(20 - 60μg/ml)可抑制VECs凋亡并抑制整合素β4表达，但不能降低血清和FGF-2缺失诱导的ROS水平。
