中国血液流变学杂志
中國血液流變學雜誌
중국혈액류변학잡지
CHINESE JOURNAL OF HEMORHEOLOGY
2013年
1期
27-30
,共4页
内皮细胞蛋白C受体%肿瘤坏死因子-α%曲格列酮%人脐静脉内皮细胞
內皮細胞蛋白C受體%腫瘤壞死因子-α%麯格列酮%人臍靜脈內皮細胞
내피세포단백C수체%종류배사인자-α%곡격렬동%인제정맥내피세포
EPCR%TNF-α%troglitazone%human umbilical vein endothelial cells
目的观察肿瘤坏死因子-α(TNF-α)及曲格列酮对人脐静脉内皮细胞(ECV304细胞)上内皮细胞蛋白C受体(EPCR)表达的影响.方法采用逆转录-聚合酶链反应(RT-PCR)检测ECV304细胞中EPCR mRNA的表达,并用流式细胞仪检测ECV304细胞中EPCR的表达量;采用实时定量PCR(Real-Time PCR)检测TNF-α及曲格列酮对ECV304细胞上EPCR mRNA表达的影响.结果 EPCR在ECV304细胞中高表达,TNF-α会下调ECV304细胞中EPCR mRNA的表达量,并呈剂量依赖性,而曲格列酮可以明显改善TNF-α对EPCR的抑制作用.结论 ECV304细胞EPCR的高表达可被TNF-α抑制,曲格列酮对TNF-α引起的抑制效应具有拮抗作用,提示曲格列酮可能对内皮细胞的损伤具有保护功能.
目的觀察腫瘤壞死因子-α(TNF-α)及麯格列酮對人臍靜脈內皮細胞(ECV304細胞)上內皮細胞蛋白C受體(EPCR)錶達的影響.方法採用逆轉錄-聚閤酶鏈反應(RT-PCR)檢測ECV304細胞中EPCR mRNA的錶達,併用流式細胞儀檢測ECV304細胞中EPCR的錶達量;採用實時定量PCR(Real-Time PCR)檢測TNF-α及麯格列酮對ECV304細胞上EPCR mRNA錶達的影響.結果 EPCR在ECV304細胞中高錶達,TNF-α會下調ECV304細胞中EPCR mRNA的錶達量,併呈劑量依賴性,而麯格列酮可以明顯改善TNF-α對EPCR的抑製作用.結論 ECV304細胞EPCR的高錶達可被TNF-α抑製,麯格列酮對TNF-α引起的抑製效應具有拮抗作用,提示麯格列酮可能對內皮細胞的損傷具有保護功能.
목적관찰종류배사인자-α(TNF-α)급곡격렬동대인제정맥내피세포(ECV304세포)상내피세포단백C수체(EPCR)표체적영향.방법채용역전록-취합매련반응(RT-PCR)검측ECV304세포중EPCR mRNA적표체,병용류식세포의검측ECV304세포중EPCR적표체량;채용실시정량PCR(Real-Time PCR)검측TNF-α급곡격렬동대ECV304세포상EPCR mRNA표체적영향.결과 EPCR재ECV304세포중고표체,TNF-α회하조ECV304세포중EPCR mRNA적표체량,병정제량의뢰성,이곡격렬동가이명현개선TNF-α대EPCR적억제작용.결론 ECV304세포EPCR적고표체가피TNF-α억제,곡격렬동대TNF-α인기적억제효응구유길항작용,제시곡격렬동가능대내피세포적손상구유보호공능.
Objective To observe effects of tumor necrosis factor-alpha(TNF-α) and troglitazone on endothelial cell protein C receptor(EPCR) expression in human umbilical vein endothelial cells(ECV304 cells),and to explore the possible mechanisms concerned.Methods EPCR expression was assessed by flow cytometry and RT-PCR in ECV304 cells.The effects of TNF-α and troglitazone were measured by Real-time PCR.Results ECV304 cells have a high expression of EPCR.TNF-α could reduce EPCR expression.However,troglitazone could significantly improve the inhibition.Conclusion We observe EPCR high expression in ECV304 cells in vitro.TNF-α can impact on EPCR expression.However,troglitazone may have a protective effect of EPCR expression on injured endothelial cells.
