缓激肽对内皮细胞分泌t-PA的影响  

The effects of bradykinin on endothelial cell secreting of t-PA

作　　者：李红霞[1] 杨向军[1] 蒋彬[1] 程绪杰[1] 陈弹[1] 宋建平[1] 刘志华[1] 蒋文平[1] 

机构地区：[1]苏州大学附属第一医院心脏病科,215006

出　　处：《江苏医药》2007年第10期976-978,共3页Jiangsu Medical Journal

基　　金：江苏省自然科学基金(BK2005034);江苏省"135"重点人才基金(RC2003019)

摘　　要：目的探讨缓激肽(BK)对纤溶系统的影响。方法培养人脐静脉内皮细胞株(ECV304),分BK刺激组,培养基中加BK至终浓度为0.01、0.1、1、10μmol/L;L-硝基-精氨酸甲酯(L-NAME)干预组,加BK(1μmol/L)后再加L-NAME至终浓度为0.1、0.2、0.5、1.0mmol/L;BK2受体拮抗剂(HOE140)干预组,加BK(1μmol/L)后再加HOE140至终浓度为1、10、100、1000nmol/L;分别测定上清中组织纤溶酶原激活物(t-PA)、纤溶酶原激活物抑制剂-1(PAI-1)、一氧化氮(NO)的含量和一氧化氮合酶(NOS)的活性。结果BK(0.1、1、10μmol/L)刺激组t-PA(ng/ml)分别为62.154±1.287、71.275±1.008、79.415±1.089,NO(μmol/L)含量分别为42.412±0.301、49.353±0.311、55.470±0.949,与对照组相比差异显著(P<0.05),而PAI-1(ng/ml)和NOS(U/ml)的活性无明显差异(P>0.05)。L-NAME干预组t-PA分别为52.401±1.121、51.903±1.202、50.126±1.401和49.362±1.209,NO含量分别为39.121±0.346、38.041±0.423、37.423±0.512和38.125±0.412,NOS活性分别为1.498±0.113、1.597±0.105、1.485±0.121和1.496±0.091,三者与空白对照组相比差异显著(P<0.05),而PAI-1含量无明显差异(P>0.05)。1000nmol/LHOE140干预后t-PA、NO含量与BK(1μmol/L)对照组相比差异显著(P<0.05),而两组PAI-1含量和NOS的活性无明显差异(P>0.05)。结论BK通过与BK2受体结合促进内皮细胞分泌t-PA,其作用是通过NO增多实现的。To investigate the effects of bradykinin（BK）and BK2 receptor antagonist（HOE140）on fibrinolytic system in ECV304（human vein endothelial cell）.Methods Cultivated ECV304 cells were stimulated with BK（0.01,0.1,1,10 μmol/L）or BK（1 μmol/L）plus NG nitro-L-arginine methyl ester（L-NAME,0.1,0.2,0.5,1 mmol/L）or BK（1μmol/L）plus HOE140（1,10,100,1000 nmol/L）for 24 hours.Tissue-type plasminogen activator（t-PA）and plasminogen activator inhibitor-1（PAI-1）in the supernatant of the cell culture were measured by enzyme linked immunosorbent assay（ELISA）.Nitric oxide（NO）was measured by nitrate reductase assay,and the activity of nitric oxide synthase（NOS）by chemical colorimetry assay.Results The concentrations of PAI-1 had no statistically significant changes whether the ECV304 cells were stimulated by BK or BK plus L-NAME or BK plus HOE140.But t-PA was significantly increased by BK from（41.117±2.901）to（62.154±1.287）,（71.275±1.008）and（79.415±1.089）ng/ml（P〈0.05）.NO was increased by BK from（34.201±0.106）to（42.412±0.301）,（49.353±0.311）and（55.470±0.949）μmol/,stimulated with BK（0.1,1,10 μmol/L）.The treatment of the combination of BK（1μmol/L）plus L-NAME significantly decreased t-PA levelfrom（71.275±1.008）to（52.401±1.121）,（51.903±1.202）,（50.126±1.401）and（49.362±1.209）ng/ml（P〈0.05）,decreased NO from（49.353±0.311）to（39.121±0.346）,（38.041±0.423）,（37.423±0.512）and（38.125±0.412）μmol/L（P〈0.05）,decreased NOS from（2.401±0.499） to （1.498±0.113）,（1.597±0.105）,（1.485±0.121）and（1.496±0.091）U/ml（P〈0.05）.BK（1μmol/L）plus HOE140（1000 nmol/L）significantly decreased the t-PA and NO level（P〈0.05）.Conclusion BK may increase t-PA through increasing NO.

关 键 词：缓激肽 BK2受体拮抗剂 组织纤溶酶原激活物 一氧化氮 

分 类 号：R322[医药卫生—人体解剖和组织胚胎学]