论文部分内容阅读
背景:脱氧核酶ED5可通过特异性抑制早期生长反应因子1的表达来阻遏下游靶基因的表达。目的:构建颈动脉损伤模型大鼠,观察早期生长反应因子1的脱氧核酶ED5对大鼠颈动脉损伤后血浆组织因子水平的影响及防治血管内膜增生的机制。方法:实验采用左颈总动脉内膜剥脱构建颈动脉球囊损伤模型大鼠,分别将ED5,MgC l2和FuG ene6注入大鼠损伤的血管节段内。结果与结论:病理学检查、免疫荧光染色、免疫组织化学染色、ELISA检测结果显示,建模后3,7,14,21 d,与MgC l2组和Fu Gene6组相比,经损伤动脉局部转染ED5后的大鼠血管组织早期生长反应因子1的表达和血浆组织因子的表达水平明显减少(P<0.01),且建模后7,14,21 d内膜增生程度明显减轻(P<0.01)。结果证实,早期生长反应因子1特异脱氧核酶ED5可能通过抑制组织因子的表达,从而抑制损伤颈动脉内膜的增生。
BACKGROUND: Deoxyribozyme ED5 can suppress the expression of downstream target genes by specifically inhibiting the expression of early growth factor 1. OBJECTIVE: To construct a rat model of carotid artery injury and observe the effect of ED5 on the level of plasma tissue factor after carotid artery injury and the mechanism of preventing and treating intimal hyperplasia. Methods: The carotid artery balloon injury models were established by carotid endarterectomy in left common carotid arteries, and ED5, MgCl2 and FuG ene6 were respectively injected into the injured vascular segments of rats. RESULTS AND CONCLUSION: Pathological examination, immunofluorescence staining, immunohistochemical staining and ELISA showed that compared with MgCl 2 group and Fu Gene 6 group, The expression of early growth factor 1 and the expression of plasma tissue factor in rat vascular tissue after ED5 were significantly reduced (P <0.01), and the degree of intimal hyperplasia was significantly reduced on the 7th, 14th and 21st day after modeling (P <0.01) ). The results confirmed that early growth factor 1-specific DNAzyme ED5 may inhibit the expression of tissue factor, thus inhibiting the injury of the carotid artery intimal hyperplasia.