论文部分内容阅读
分析Ca2+通道相关关键基因在大鼠创伤性肢体深静脉血栓形成中的表达变化,初步探讨该信号通路在此病理过程中的生物学意义。采用定量击打双侧大腿+双后肢石膏固定的方式,对150只SD大鼠造模,建立创伤性深静脉血栓形成动物模型。应用Genechip Rat Genome 430 2.0芯片,检测创伤性深静脉血栓形成过程中8种不同生物学状态下(正常对照、创伤即刻、血栓形成初始期、高峰期血栓形成、高峰期血栓不形成、血栓消退、血栓不消退、血栓不形成)股静脉RNA表达情况,筛查出差异表达基因,并进行pathway分析。重点关注高峰期血栓形成与不形成两种生物学状态下C,a2+通道相关关键基因表达变化。结果显示:高峰期血栓形成组与不形成组比较,Ca2+通道中CaMK、IP3 3K、CaN等多个关键基因表达均呈现下调,可能使包括内皮细胞在内的多种血管细胞,增殖、分化、代谢等功能受到抑制,并影响下游信号通路,引起组织细胞功能失调,最终导致血栓发生。因此,推测Ca2+通道功能受抑制可能与TDVT发生有关。
To analyze the expression changes of Ca2 + channel-related key genes in deep venous thrombosis of traumatic limbs in rats and to explore the biological significance of this signaling pathway in this pathological process. A total of 150 Sprague-Dawley rats were modeled by double-sided thigh + double hind limb plaster fixation to establish a traumatic deep vein thrombosis animal model. The Genechip Rat Genome 430 2.0 chip was used to detect 8 different biological states during traumatic deep vein thrombosis (normal control, immediate traumatic injury, initial thrombosis, peak thrombosis, peak thrombosis, thrombosis subsided, Thrombosis does not subside, thrombosis does not form) femoral vein RNA expression, screening of differentially expressed genes, and pathway analysis. Focus on peak thrombosis and non-formation of two biological states of C, a2 + channel-related key gene expression changes. The results showed that the expressions of CaMK, IP3 3K, CaN and other key genes in Ca2 + channels were down-regulated in peak thrombosis and non-formation groups, which may result in the proliferation, differentiation, differentiation of multiple vascular cells including endothelial cells, Metabolism and other functions are inhibited, and affect the downstream signaling pathway, causing tissue dysfunction, eventually leading to thrombosis. Therefore, it is speculated that the inhibition of Ca2 + channel function may be related to the occurrence of TDVT.