探讨血管紧张素Ⅱ对人脐静脉内皮细胞产生超氧阴离子和1
型纤溶酶原激活物抑制剂的作用机制
叶国红;韩莲花;李红霞;蒋文平;戴海鹰;李勋
【期刊名称】《中国循环杂志》 【年(卷),期】2012(027)002
【摘要】目的:探讨血管紧张素Ⅱ(AngⅡ)对人脐静脉内皮细胞(HUVECs)产生超氧阴离子(O-2)和1型纤溶酶原激活物抑制剂( PAI-1)的作用机制及0-2与PAI-1产生之间的关系.方法:第一部分实验:观察血管紧张素Ⅱ不同浓度及不同作用时间对HUVEcs产生0-2和PAI-1的作用.分为对照组,AngⅡ10-8～10-5 moL/L不同浓度组,AngⅡ10-6mol/L作用不同时间(0、6、12、24和48h).第二部分实验:观察不同浓度的缬沙坦对AngⅡ诱导HUVECs产生O-2和PAI-1的作用.分为对照组,缬沙坦(10-6 mol/L)组,AngⅡ(10-6mo/L)组,AngⅡ(10-6mol/L)+不同浓度缬沙坦(10-8～ 10-5mol/L)组.第三部分实验:观察缬沙坦、二甲苯基碘、超氧化物歧化酶对AngⅡ使HUVECs产生O-2和PAI-1的作用.分为对照组,AngⅡ(10-6 mol/L)组,AngⅡ(10-6 mol/L)+缬沙坦(10-6mol/L)组,AngⅡ(10-6mol/L)+二甲苯基碘(10μmol/L)组,AngⅡ(10-6mol/L)+超氧化物歧化酶(2μl)组.用酶消化法收集并培养HUVECs,采用氯化硝基四氮唑蓝还原法测定上清液O-2浓度,用酶联免疫吸附法测定上清液PAI-1浓度.结果:①AngⅡ在10-8～10-5mol/L范围内呈浓度依赖性地使HUVECs产生O-2和PAI-1增加.②缬沙坦在10-8～10-5mol/L范围内呈浓度依赖性地降低AngⅡ促HUVECs产生O-2和P1AI-1的作用.③二甲苯基碘和超氧化物歧化酶可显著抑制AngⅡ刺激HUVECs产生0-2及PAI-1.结论:①AngⅡ通过作用
于AngⅡ受体1(AT1)激活还原型辅酶Ⅱ(NADPH)氧化酶途径呈浓度和时间依赖性地使HUVECs产生O-2和PAI-1增加.②AngⅡ通过增加O-2产生而致PAI-1产生增加,提示抗氧化治疗有助于预防血栓性疾病的发生.%Objective: To investigate the effect of angiotensin D (Ang II) on super oxide anions (O2) and plasminogen activator inhibitor-1 (PAI-1) production in human umbilical vein endothelial cells (HUVECs) with its mechanism,and to explore the relationship between O2- and PAI-1 production.Methods: ①To observe Angfl on O2- and PAI-1 production in HUVECs at different concentrations and times. HUVECs were incubated with AngII from (10-7 to 10-5) mol/L for 24 hours.and HUVECs were incubated with AngII 10-6 mol/L for (0,6,12,24 and 48) hours. ②To observe different doses of valsartan on Angll induced O2- and PAI-1 production in HUVECs. AngII 10-6 mol/L pretreated HUVECs were incubated with valsartan (10-8 to 10-5) mol/L. ③To respectively observe valsartan,diphenvleoe iodonium (DPI) and super oxide dismutase (SOD) an Angll induced 0, and PAI-1 production. Angll pretreated HUVECs were respectively incubated with valsartan10-6 mol/L,with DPI 10 μmal/L and with SOD 2 μl. Control group was set up in each experiment. The product PA1-1 level was examines by ELISA and O2- level was measured by nitroblne tetrazolium (NBT) method. Results: ①At the rage of (10-8 to10-5) mol/L, Ang II increasing PAI-1 and O2- production in HUVECs in a dose- and time-dependent manner. ②At the rage of (10-8 to10-5) mol/L, valsartan
decreasing Ang II induced PAI-1 and O2- production in a dose-dependent manner. ③DPI and SOD can also suppress Ang II induced PAI-1 and O2- production. Conclusion: ① Ang II promotes PAI-1 and O2- production through Ang II receptor 1 activated NADPH oxidase pathway. ②Ang II increasing PAI-1 production through the increased O2-, which implies that antioxidant therapy may prevent thrombosis. 【总页数】4页(141-144)
【关键词】血管紧张素Ⅱ;脐静脉内皮细胞;超氧阴离子;1型纤溶酶原激活物抑制剂
【作者】叶国红;韩莲花;李红霞;蒋文平;戴海鹰;李勋
【作者单位】410007湖南省长沙市,长沙市中心医院心内科;苏州大学附属第一医院心内科;苏州大学附属第一医院心内科;苏州大学附属第一医院心内科;410007湖南省长沙市,长沙市中心医院心内科;苏州大学附属第一医院心内科 【正文语种】中文 【中图分类】R54 【文献来源】
https://www.zhangqiaokeyan.com/academic-journal-cn_chinese-circulation-journal_thesis/0201232045815.html 【相关文献】
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探讨血管紧张素Ⅱ对人脐静脉内皮细胞产生超氧阴离子和1型纤溶酶
