CAJ | 학술논문

目的：观察肿瘤坏死因子-α（ tumor necrosis factor-α，TNF-α）对人脐静脉内皮细胞（ HUVECs）组织型纤溶酶原激活物（tissue plasminogen activitor，t-pA）及其抑制剂-1（plasminogen activitor inhibitor-1，pAI-1）表达的影响。方法：原代分离HUVECs细胞并进行传代培养，分别以6个TNF-α浓度组（0、1、10、20、50、100 ng·mL-1）处理不同时间（0、1、3、6、12、24 h），酶联免疫吸附分析（ ELISA）法测定t-pA、pAI-1抗原的表达；逆转-聚合酶链反应（ RT-pCR）检测t-pA、pAI-1基因的表达。结果：TNF-α促进pAI-1抗原的表达，并呈剂量和时间依赖关系，在 TNF-α10 ng·mL-1作用6 h时最明显（ p<0.01）；TNF-α促进pAI-1 mRNA的表达，并呈剂量和时间依赖关系，在TNF-α10 ng·mL-1作用3 h时已非常明显（p<0.01），6 h时达到高峰（p<0.01）；而TNF-α对HUVECs表达t-pA抗原、mRNA无明显影响。结论：炎症因子TNF-α可能通过上调pAI-1表达而诱发血栓相关疾病。
목적：관찰종류배사인자-α（ tumor necrosis factor-α，TNF-α）대인제정맥내피세포（ HUVECs）조직형섬용매원격활물（tissue plasminogen activitor，t-pA）급기억제제-1（plasminogen activitor inhibitor-1，pAI-1）표체적영향。방법：원대분리HUVECs세포병진행전대배양，분별이6개TNF-α농도조（0、1、10、20、50、100 ng·mL-1）처리불동시간（0、1、3、6、12、24 h），매련면역흡부분석（ ELISA）법측정t-pA、pAI-1항원적표체；역전-취합매련반응（ RT-pCR）검측t-pA、pAI-1기인적표체。결과：TNF-α촉진pAI-1항원적표체，병정제량화시간의뢰관계，재 TNF-α10 ng·mL-1작용6 h시최명현（ p<0.01）；TNF-α촉진pAI-1 mRNA적표체，병정제량화시간의뢰관계，재TNF-α10 ng·mL-1작용3 h시이비상명현（p<0.01），6 h시체도고봉（p<0.01）；이TNF-α대HUVECs표체t-pA항원、mRNA무명현영향。결론：염증인자TNF-α가능통과상조pAI-1표체이유발혈전상관질병。
Objective:To observe the effects of tumor necrosis factor-α( TNF-α)on the tissue plasminogen activator( t-pA )and plasminogen activitor inhibitor-1( pAI-1 )expression in human umbilical vein endothelial cells( HUVEC ). Meth-ods:Original HUVECs cell were isolated and subcultured. They were divided into six TNF-α concentration groups(0,1, 10,20,50,100 ng·mL-1)and were dealt with in different hours(0,1,3,6,12,24 h). The expressions of T-pA and pAI-1 antigen were determined by ELISA;t-pA mRNA and pAI-1 mRNA were examined by reverse transcription polymer-ase chain reaction( RT-pCR). Results:TNF-α promoted pAI-1 antigen expression in HUVECs in a dose or time inde-pendent manner,reaching a maximum level with TNF-α10 ng·mL-1 after 6 hours(p<0. 01);TNF-α promoted pAI-1 mRNA expression in HUVECs in a dose or time independent manner,being fairly apparent with TNF-α10 ng·mL-1 af-ter 3 hours(p<0. 01)and reaching a maximum level with TNF-α10 ng·mL after 6 hours(p<0. 01);There were no effect on the t-pA antigen and mRNA exprssion induced by TNF-αin HUVECs. Conclusion:TNF-αmay induce thrombo-sis related diseases by enhancing pAI-1 expression.