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目的:探讨细胞外信号调节激酶1/2(ERK1/2)在高血压大鼠模型动脉外膜血管重塑中的作用。方法:利用血管紧张素II(Ang II)微泵灌注制备高血压大鼠模型,随机分为未处理组、生理盐水灌注组和Ang II灌注组。分别检测各组大鼠尾动脉收缩压及血管形态学改变;Western blotting技术检测外膜成纤维细胞过氧化氢酶(CAT)蛋白在未处理组、单纯Ang II、ERK1/2抑制剂PD98059和Ang II+PD98059培养下的表达。结果:大鼠颈动脉HE染色和收缩压结果显示,与未处理组及生理盐水灌注组相比,Ang II组大鼠颈动脉中膜厚度和收缩压明显增加(P<0.01),动脉形态结构有明显改变,并且有显著的病理性血管重塑发生。Western blotting检测结果显示,PD98059作用下CAT比单纯Ang II明显增高(P<0.05),表明ERK1/2信号通路能够恢复Ang II诱导的CAT表达下调。结论:Ang II可能通过ERK1/2信号通路下调血管外膜CAT的表达,进而促进血管细胞表型转化,导致血管病理性重塑发生。
AIM: To investigate the role of extracellular signal-regulated kinase 1/2 (ERK1 / 2) in the remodeling of adventitial vessels in hypertensive rat models. Methods: Hypertensive rats were prepared by microinjection of angiotensin II (Ang II) into rat models of hypertension and were randomly divided into untreated group, normal saline group and Ang II group. The tail artery systolic pressure and morphological changes of blood vessels in each group were detected. Western blotting was used to detect the expression of catalase (CAT) in outer membrane fibroblasts in untreated group, Ang II alone, ERK1 / 2 PD98059 and Ang Ⅱ II + PD98059. Results: HE staining and systolic blood pressure of carotid arteries in rats showed that carotid intima-media thickness and systolic pressure increased significantly in Ang II group compared with those in untreated group and normal saline group (P <0.01). Arterial morphology Significant changes, and significant pathological vascular remodeling occurred. The results of Western blotting showed that the CAT level in PD98059 group was significantly higher than that of Ang II alone group (P <0.05), indicating that the ERK1 / 2 signaling pathway could restore the down regulation of CAT induced by Ang II. CONCLUSIONS: Ang II may down-regulate the expression of CAT in the adventitia by ERK1 / 2 signaling pathway, thereby promoting angiogenesis and angiogenesis.