CAJ | 학술논문

背景:深静脉血栓形成及消退过程中的分子机制极其复杂,目前已有研究表明,缺氧与损伤因素参与了深静脉血栓形成及消退过程.目的:观察静脉壁中缺氧诱导因子1在创伤性深静脉血栓模型兔血栓形成及消退过程中的表达变化.方法:将日本大耳白兔采用钳夹双侧股静脉+石膏固定双下肢建立兔创伤性深静脉血栓模型.PCR及ELISA检测股静脉组织中缺氧诱导因子1 mRNA、蛋白在兔创伤性深静脉血栓建模后表达的变化.结果与结论:模型兔创伤后24 h,经 B超监测,血栓形成率为58%;血栓栓子随造模后时间延长逐渐缩小机化,创伤后第5天开始经B超监测模型组血栓形成的血管腔有断续血流信号.模型兔股静脉组织中缺氧诱导因子1在造模后1,3,5 d表达逐渐升高(P<0.05或P<0.01),此后7-14 d 表达逐渐下降(P <0.05或 P <0.01).结果证实,在创伤性深静脉血栓形成过程,缺氧诱导因子1表达上调,在血栓形成后的溶解及机化再通过程中,缺氧诱导因子1表达下调.
배경:심정맥혈전형성급소퇴과정중적분자궤제겁기복잡,목전이유연구표명,결양여손상인소삼여료심정맥혈전형성급소퇴과정.목적:관찰정맥벽중결양유도인자1재창상성심정맥혈전모형토혈전형성급소퇴과정중적표체변화.방법:장일본대이백토채용겸협쌍측고정맥+석고고정쌍하지건립토창상성심정맥혈전모형.PCR급ELISA검측고정맥조직중결양유도인자1 mRNA、단백재토창상성심정맥혈전건모후표체적변화.결과여결론:모형토창상후24 h,경 B초감측,혈전형성솔위58%;혈전전자수조모후시간연장축점축소궤화,창상후제5천개시경B초감측모형조혈전형성적혈관강유단속혈류신호.모형토고정맥조직중결양유도인자1재조모후1,3,5 d표체축점승고(P<0.05혹P<0.01),차후7-14 d 표체축점하강(P <0.05혹 P <0.01).결과증실,재창상성심정맥혈전형성과정,결양유도인자1표체상조,재혈전형성후적용해급궤화재통과정중,결양유도인자1표체하조.
BACKGROUND:The molecular mechanism of deep vein thrombosis and further regression is extremely complex. Researches show that hypoxia and injury factors are involved in deep vein thrombosis and regression. OBJECTIVE:To investigate changes in hypoxia inducible factor (HIF)-1 expression during deep vein thrombosis and regression in a rabbit model of traumatic deep vein thrombosis (TDVT). METHODS:The bilateral femoral vein of rabbits was clamped and both lower extremities were fixed with gypsum to establish model of TDVT. SYBR?Green I fluorescence real-time quantitative PCR and ELISA dynamic detection were used to determine the change of HIF-1 mRNA and protein expression in femoral vein in the rabbits with TDVT. RESULTS AND CONCLUSION:At 24 hours post-injury, B-ultrasonography showed that thrombosis rate was 58%and thromboembolus gradual y reduced and be organized with time;from the 5th day intermittent flow signals were monitored in lumen of blood vessel with thrombosis of model group. HIF-1 expression in vein of model group gradual y increased (P<0.05 or P<0.01), and reduced between 7-14 days (P<0.05 or P<0.01). Those findings indicate that HIF-1 expression is upregulated during TDVT, but downregulated during thrombolysis and organization.