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目的:探讨Jak蛋白酪氨酸激酶-信号转导子和转录激活子信号通路在创伤性深静脉血栓形成中的作用。方法:将150只SD大鼠随机分为正常对照(A组)和模型组。模型组根据造模后的不同生物学状态再分为7组:创伤即刻(B组)、血栓形成前期(C组)、高峰期血栓形成(D组)、高峰期血栓不形成(H组)、血栓消退期(E组)、血栓不消退(F组)和血栓不形成(G组),在相应时相点无创切取股静脉血管组织,随后抽取各组大鼠总RNA,用Genechip Rat Genome430 2.0芯片测定股静脉RNA表达,并分析Jak蛋白酪氨酸激酶-信号转导子和转录激活子信号通路基因表达变化情况。结果:Jak蛋白酪氨酸激酶-信号转导子和转录激活子信号通路中Cytokine R、STAT、PI3K、AKT、SOCS、CycD等关键基因均呈下调,调控着细胞凋亡、细胞周期等。结论:Jak蛋白酪氨酸激酶-信号转导子和转录激活子信号通路可能是调控血栓的生物学状态的重要信号通路之一。
Objective: To investigate the role of Jak protein tyrosine kinase - signal transducer and activator of transcription pathway in traumatic deep vein thrombosis. Methods: 150 SD rats were randomly divided into normal control (group A) and model group. The model group was further divided into 7 groups according to the different biological states after modeling: immediate trauma (group B), pre-thrombosis (group C), peak thrombosis (group D), peak thrombosis (group H) (E group), thrombus did not subside (F group) and thrombus did not form (G group). At the corresponding time points, the femoral vein tissue was obtained by noninvasive extraction. The total RNA of each group was extracted and the total RNA was extracted with Genechip Rat Genome 430 2.0 chip to measure the expression of femoral vein RNA, and analyze the expression of Jak protein tyrosine kinase signal transducers and activators of transcription pathway. Results: The key genes of Cytokine R, STAT, PI3K, AKT, SOCS and CycD in Jak protein tyrosine kinase - signal transducers and transcriptional activator signaling pathways were downregulated, which regulated apoptosis and cell cycle. Conclusion: The Jak protein tyrosine kinase - signal transducer and activator of transcription signaling pathways may be one of the important signal pathways that regulate the biological status of thrombus.