摘要
目的本研究旨在观察体外条件下晚期糖基化终产物(AGE)诱导内皮细胞凋亡机制以及黄芪的影响。方法体外培养人冠状动脉内皮细胞,根据AGE诱导内皮细胞凋亡的有效浓度,分为正常对照组、AGE剌激组、AGE剌激加低、中、高浓度黄芪多糖组(终浓度分别为100、200和400 mg/L)。MTS方法分析细胞增殖率,激光共聚焦检测细胞内氧自由基ROS变化及用ELISA法检测人凋亡相关因子FAS水平。结果①AGE修饰的人血清白蛋白可以诱导血管内皮细胞凋亡,呈浓度依赖,而中、高浓度黄芪多糖可以抑制该作用(P<0.01);②黄芪多糖可下调AGE诱导的ROS水平;③AGE组可促使血管内皮细胞FAS分泌明显升高(P<0.01),中、高浓度黄芪多糖可降低AGE诱导FAS的水平,在400 mg/L浓度最明显,且与ROS抑制剂NAC比较差异无显著性(P>0.05)。结论黄芪可抑制晚期糖基化终产物诱导内皮细胞凋亡,其效应可能与ROS通路相关。
Objective To investigate the effect of astragalus polysaccharides （APS） on advanced glycation end-products （AGE） induced endothelial cells apoptosis. Methods Human coronary artery endothelial cells （HCAECs） were cultured in vitro and effective concentration of AGE induced apoptosis were measured by MTS. Cell were divided into 5 groups： control group （20 mg/L）, AGE group （20 mg/L）, and AGE with low, middle and high A PS groups. Cell apoptosis were determined by MTS analysis, ROS were detected and further evaluated by Zeiss LSM710 confocal microscope, FAS/CD95 level in cell culture supernatant were detected by ELISA. Results Compare with control group, AGE significantly induced cell apoptosis on dose dependent manner, middle or high-APS could inhibit those effects by down-regnlate AGE induced ROS level （P 〈0.01）; Furthermore, middle or high-APS decrease AGE induced FAS secretion and high-APS achieved the maximal effect which was no significant differences compare with ROS inhibitor NAC. Conclusions A strogalus polysaccharides protects advanced glycation end-products induced endothelial cells apoptosis by down-regulate ROS generation and suppress FAS level.
出处
《临床医学工程》
2014年第1期18-20,共3页
Clinical Medicine & Engineering
基金
广州市中医药
中西医结合立项科研课题(项目编号:2009-A-41)
关键词
黄芪多糖
晚期糖基化终产物
凋亡
动脉粥样硬化
A stragalus polysaccharides
Advanced glycation end-products
Apoptosis
Atherosclerosis
