红花黄色素B对AngⅡ诱导内皮细胞线粒体损伤的保护作用

血管内皮细胞(vascular endothelial cell,VEC)作为血液与组织之间的屏障,参与多种生理和病理过程,其功能异常与动脉粥样硬化、高血压、糖尿病等有紧密的联系[1?4]。血管紧张素Ⅱ(angiotensin-Ⅱ,Ang-Ⅱ)可促进内皮细胞内活性氧自由基(reactiveoxygen species,ROS)的生成,改变胞内Ca2+

Effect of safflor yellow B on vascular endothelial cells injury induced by angiotensin-II

This study is to investigate protective effect of safflor yellow B (SYB) against vascular endothelial cells (VECs) injury induced by angiotensin-II (Ang-II). VECs were cultured and divided into six groups: control group, Ang-II group, Ang-II + SYB (1 micromolL(-1)) group, Ang-II + SYB (10 micromolL(-1)) group, Ang-II + SYB (100 micromolL(-1)) group and Ang- II + verapamil (10 micromolL(-1)) group. Except control group, all of VECs in other groups were treated with Ang- II at the final concentration of 0.1 micromolL(-1). Mitochondria membrane potential (MMP) and free calcium concentration ([Ca2+]i) were measured by laser scanning confocal microscopy, and mitochondria complex IV activity was detected by BCA method. The levels of reactive oxygen species (ROS) in VECs were analyzed by fluorescence detector and apoptosis of VECs was observed by flow cytometer. Caspase 3 was determined by Western blotting method. Comparing with control group, Ang-II was able to increase [Ca2+]i and ROS level, decrease MMP level, inhibit complex IV activity and enhance caspase 3 activity in VECs, as a result, enhance apoptosis of VECs. But SYB could significantly reduce the result induced by Ang- II relying on different dosages (P < 0.05 or P < 0.01). SYB was able to eliminate the effect of Ang-II on VECs via regulating [Ca2+]i, mitochondrial structure and function and inhibiting apoptosis.