黄芪多糖组分-A3对对氧磷所致血管内皮功能损伤的保护作用  

Protective Effects of APS-A3 on Blood Vessel Endothelium Function Induced by Paraoxon

作　　者：尹雅玲[1] 李鹏[2] 卢光洲[2] 梁金英[2] 赵繁荣[2] 

机构地区：[1]新乡医学院.基础医学院,河南新乡453003 [2]新乡医学院.药学院,河南新乡453003

出　　处：《时珍国医国药》2011年第3期583-585,共3页Lishizhen Medicine and Materia Medica Research

基　　金：河南省教育厅自然科学研究计划项目(No.2010B330002)

摘　　要：目的观察黄芪多糖组分-A3(APS-A3)对对氧磷(PARA)所致血管内皮功能损伤的保护作用。方法以大鼠离体胸主动脉血管环(EVAPVR)和培养的人脐静脉内皮细胞(HUVEC)为实验对象,以PARA为损伤药物,以APS-A3为保护药,检测血管内皮依赖性舒张反应(EDRR)、内皮细胞单层通透性(ECMP)及细胞培养液生化指标。结果 APS-A3剂量依赖性(0.1,1,10 mg/ml)地显著减轻了PARA(3.63μmol/L)对血管EDRR的抑制作用,降低了ECMP的增加,保护了超氧化物歧化酶(SOD)活性、阻滞了丙二醛(MDA)浓度的升高以及一氧化氮(NO)浓度的降低(均P<0.05)。结论 APS-A3对PARA所致的血管内皮功能损伤有明显的保护作用,其机制可能与APS-A3的抗氧化作用有关。Objective To observe the protective effects of APS-A3 on blood vessel endothelium function induced by paraoxon（PARA）. Methods The ex vivo aorta pectoralis vascular ring（EVAPVR） of rats and cultured human umbilical vein endothelial cells（HUVEC） were exposed to medium contained paraoxon（3.63 μmol/L）,APS-A3 for difference concentration were used to inhibit the damage effect.The endothelial-dependent relaxation reaction（EDRR）,endothelial cell monolayer permeability（ECMP）,biochemical index were measured. Results APS-A3 dose dependently（0.1,1,10 mg/ml） reduced the inhibition of ACh-induced EDRR and the increased ECMP induced by PARA,simultaneously APS-A3（10 mg/ml） also protected the SOD activity,inhibited the increase of the MDA content and reduction of NO content induced by PARA in medium of cultured HUVEC. Conclusion APS-A3 can protect the blood vessel endothelium function impaired by PARA,and the potential mechanism is possibly concerned with the antioxidation of APS-A3.

关 键 词：黄芪多糖 对氧磷 内皮细胞 氧化 

分 类 号：R932[医药卫生—生药学]