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作 者:郝冉冉[1] 王晨静[2] 仲伟珍[1] 夏蕴秋[1] 韩彦弢[1]
机构地区:[1]青岛大学医学院,青岛266071 [2]青岛大学医学院附属医院,青岛266071
出 处:《中药药理与临床》2014年第4期29-32,共4页Pharmacology and Clinics of Chinese Materia Medica
基 金:国家自然基金(No 81173593)
摘 要:目的:复制氧化性低密度脂蛋白(oxidized low density lipoprotein,ox-LDL)诱导的人脐静脉内皮细胞(Human Umbilical Vein Endothelial Cells,HUVECs)氧化损伤模型,并探讨熊果酸(Ursolic Acid,UA)对其保护作用。方法:以体外培养的HUVECs为实验对象,采用不同浓度(5,10,15,20μM)熊果酸及阳性对照药物维生素E预处理细胞16 h,再加入100μg/ml的ox-LDL培养24 h造成细胞氧化损伤。CCK-8检测细胞存活率,酶联免疫法检测各组细胞培养上清液过氧化氢(H2O2)、一氧化氮(NO)、丙二醛(MDA)含量,超氧化物歧化酶(SOD)活力以及各组细胞裂解液中一氧化氮合成酶(NOS)活力;采用SPSS 17.0软件对实验数据进行统计学分析。结果:与正常组相比,模型组细胞存活率、NO、SOD、NOS水平明显降低,MDA、H2O2水平明显增加;与模型组比较,熊果酸在5-20μM范围内,呈剂量依赖性提高细胞存活率,上调NO、SOD、NOS水平,并下调MDA、H2O2水平。结论:100μg/ml的ox-LDL能够诱导HUVECs发生氧化损伤,熊果酸能够通过抗氧化发挥保护作用,其机制可能与维持NOS、SOD活性、减少MDA、H2O2生成等有关。To investigate the protective effects and mechanisms of ursolic acid on damaged umbilical vein endothelial cells (HUVECs) induced by ox-LDL. Methods: HUVECs were administered with different concentrations(5,10,15,20 μM) of UA for 16 h. Then they were treated with 100 ? g/ml ox-LDL for 24 h to duplicate an oxidative injury model. The cell viability of HUVECs was detected by CCK-8. The content of hydrogen peroxide ( H2O2 ), nitric oxide ( NO), malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) and ni- tric oxide synthase (NOS) were detected by enzymic method. The experimental data was statistical analysised by SPSS 17.0. Results: Com- pared with the control group, the cell viability, NO, SOD, NOS levels in model group were significantly declined while the MDA, H2 O2 lev- els were significantly increased ( P 〈 0.05). Compared with the model group, UA could improve the cell viability, increase the NO, SOD, NOS levels and lower the MDA, H2 O2 levels in a dose-dependent manner. Conclusion: 100μg/ml ox-LDL could induce oxidative damage of HUVECs, and UA could play a protective role through its anti-oxidative effect. This may be related to its effect of maintaining NOS, SOD ac- tivity, reducing MDA, H2O2 generation and so on.
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