丹参酸A通过调控血管内皮细胞谷胱甘肽过氧化物酶活性及丙二醛含量抑制内毒素诱导的凋亡(英文)  

Salvianic acid A inhibits lipopolysaccharide-induced apop-tosis through regulating glutathione peroxidase activity and malondialdehyde level in vascular endothelial cells

作　　者：赵启韬[1] 郭庆梅[2] 王鹏[2] 王倩[1] ZHAO Qi-Tao;GUO Qing-Mei;WANG Peng;WANG Qian(Laboratory of Cytobiology,School of Basic Medicine,Shandong University of Traditional Chinese Medicin,Jinan,250355,China;Department of Pharmacognos,School of Pharmaceutical Sciences,Shandong University of Traditional Chinese Medicin,Jinan,250355,China)

机构地区：[1]山东中医药大学基础医学院,济南250355 [2]山东中医药大学药学院,济南250355

出　　处：《中国天然药物》2012年第1期53-57,共5页

基　　金：supported by the Incentive Foundation for Outstanding Young and Middle-aged Scientists of Shandong Province,China (No. 2006BS03047)~~

摘　　要：目的:探寻丹参素 (丹参酸 A, SAA)对脂多糖(LPS)处理的血管内皮细胞 (VEC) 的保护作用及可能机制。方法:以 LPS 处理培养的人脐静脉血管内皮细胞, 造成细胞凋亡, 培养液中同时加入系列浓度的 SAA; 倒置相差显微镜观察细胞形态变化; 吖啶橙染色+激光共聚焦显微镜观测凋亡小体; PI 染色+流式细胞仪测定细胞周期分布; MTT 法检测细胞存活率; 生化试剂盒检测细胞内谷胱甘肽脱氢酶(GSH-Px) 活性及丙二醛(MDA)水平。结果:SAA 可明显抑制细胞凋亡, 提高细胞存活率。且该作用具浓度依赖性。对于 LPS 导致的细胞周期异常、GSH-Px 活性下降、MDA 水平升高, SAA 均可明显逆转。结论:丹参酸 A 通过抗氧化作用抑制内毒素诱导的血管内皮细胞凋亡。AIM： To find out the role of salvianic acid A （SAA） in the protection of vascular endothelial cells （VEC） and its possi- ble mechanism in vitro. METHODS： The ingredient at various concentrations was added to human umbilical vein endothelial cells （HUVEC） treated with 0.5 μmol L-1 lipopolysaccharide （LPS） for 24 h. Apoptotic morphological changes of cells were observed under inverted phase contrast microscope; the cell viability was quantified using MTT assay. Nuclear fragmentation of cells was observed under laser scanning confocal microcope after being stained with acridinorange. Cell cycle distribution was detected by flow-cytometry after being stained with propidium iodide （PI）. The activities of glutathione peroxidase （GPH-PX） as well as maleic dialdehyde （MDA） level in cells were measured by spectrophotometric methods as described in the assay kits. RESULTS： Apoptotic morphological changes and the decrease of cell viability of these cells were obviously inhibited by SAA in a dose-dependent manner. Furthermore, the abnormal cell cycle distribution, the decrease of GSH-Px activity and the increase of MDA level induced by LPS were markedly reversed. CONCLUSION： SAA exerts protective effect on VEC induced by LPS via an antioxidative mechanism.

关 键 词：丹参素 血管内皮细胞 内毒素 谷胱甘肽过氧化物酶 丙二醛 

分 类 号：R965[医药卫生—药理学]