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目的:探讨依维莫司对大鼠颈总动脉球囊损伤模型增生内膜的影响及其可能作用机制。方法:健康雄性SD大鼠36只,随机分为假损伤组(对照组)、颈总动脉球囊损伤组(损伤组)和颈总动脉球囊损伤+口服依维莫司组(依维莫司组),每组12只。依维莫司组于颈总动脉球囊损伤前1天,用依维莫司负荷剂量1.5 mg/kg灌胃,随后给予其剂量0.75 mg.kg-1.d-1灌胃直至第28天,对照组与损伤组给予等量0.9%氯化钠溶液灌胃。各组均于术后第28天取颈总动脉损伤段,观测颈动脉形态学变化,以免疫组化法测定损伤血管内膜真核翻译起始因子4E(eIF-4E)及增殖细胞核抗原(PCNA)的表达情况。结果:对照组血管内膜无增生,eIF-4E、PCNA表达极少;与对照组比较,损伤组新生内膜形成并增生明显,eIF-4E、PCNA表达显著增强;依维莫司组较损伤组新生内膜增生减轻,eIF-4E及PCNA表达明显降低,差异有统计学意义(P<0.05)。结论:依维莫司可抑制大鼠颈总动脉球囊损伤模型新生内膜增殖.其作用机制可能与抑制eIF-4E及PCNA表达有关。
Objective: To investigate the effect of everolimus on the proliferative endothelium of carotid artery balloon injury model in rats and its possible mechanism. Methods: Thirty-six healthy male Sprague-Dawley rats were randomly divided into sham injury group (control group), common carotid artery balloon injury group (injured group), common carotid artery balloon injury + oral everolimus group Secretary group), each group of 12. The everolimus group was orally administered with everolimus loading dose of 1.5 mg / kg one day prior to the common carotid artery balloon injury, followed by intragastric administration of its dose of 0.75 mg.kg-1.d-1 until day 28 , The control group and the injury group given the same amount of 0.9% sodium chloride solution gavage. The injury of common carotid artery was taken on the 28th day after operation and the morphological changes of the carotid artery were observed. The expressions of eIF-4E and proliferating cell nuclear antigen (eIF-4E) were detected by immunohistochemistry PCNA) expression. Results: Compared with the control group, neointimal hyperplasia was found in the injured group and the expression of eIF-4E and PCNA was significantly increased in the control group. There was no significant difference in the expression of eIF-4E and PCNA between the two groups In neointimal hyperplasia, the expression of eIF-4E and PCNA were significantly reduced in group B, with a significant difference (P <0.05). Conclusion: Everolimus can inhibit neointimal hyperplasia in carotid artery balloon injury model in rats, which may be related to the inhibition of eIF-4E and PCNA expression.