Zhou H, Liu X, Liu L, Yang Z, Zhang S, Tang M, Tang Y, Dong Q, Hu R
Department of Neurology, Huashan Hospital, Fudan University, Shanghai, China; Department of Neurology, Changshu Hospital, Yangzhou University, Changshu, China.
J Int Med Res. 2009 Nov-Dec;37(6):1897-903. doi: 10.1177/147323000903700627.
Damage to endothelial cells is a key event in the pathogenesis of atherosclerosis and vascular disease. This study aimed to determine whether free fatty acids (FFAs) induced oxidative stress and apoptosis in human brain microvascular endothelial cells (HBMVECs) in vitro and, if so, which signalling pathway mediated these effects. After culture in different concentrations of FFAs for 24 - 72 h, cell viability/proliferation was determined using a cell counting kit, apoptosis was detected by measuring caspase-3 activity and by using annexin V-conjugated fluorescein isothiocyanate/propidium iodide staining, and oxidative stress was evaluated by measuring the levels of reactive oxygen species (ROS) and mitochondrial membrane potential (MMP). The HBMVECs exposed to FFAs showed significantly decreased cell proliferation, increased apoptosis and ROS levels, and decreased MMP. In conclusion, the results showed that high levels of FFAs induced oxidative stress, which damaged HBMVECs and resulted in apoptosis.
内皮细胞损伤是动脉粥样硬化和血管疾病发病机制中的关键事件。本研究旨在确定游离脂肪酸（FFA）是否在体外诱导人脑血管内皮细胞（HBMVEC）发生氧化应激和凋亡，如果是，哪种信号通路介导了这些效应。在不同浓度的FFA中培养24 - 72小时后，使用细胞计数试剂盒测定细胞活力/增殖，通过测量caspase-3活性以及使用膜联蛋白V偶联异硫氰酸荧光素/碘化丙啶染色检测凋亡，并通过测量活性氧（ROS）水平和线粒体膜电位（MMP）评估氧化应激。暴露于FFA的HBMVEC显示细胞增殖显著降低、凋亡和ROS水平增加以及MMP降低。总之，结果表明高水平的FFA诱导氧化应激，损伤HBMVEC并导致凋亡。
