血管紧张素(17)对氧化低密度脂蛋白诱导大鼠主动脉内皮细胞损伤的作用机制

来源 :中西医结合心脑血管病杂志 | 被引量 : 0次 | 上传用户:hubai123
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目的观察血管紧张素(1-7)[Ang(1-7)]对氧化低密度脂蛋白(ox-LDL)诱导的大鼠主动脉内皮细胞(SVAREC)血凝素样氧化型低密度脂蛋白受体1(LOX-1)、细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)表达水平的影响,探讨其可能作用机制。方法将大鼠随机分为ox-LDL组和ox-LDL+Ang(1-7)组。实验通过Cell Counting Kit-8(简称CCK-8)检测细胞增殖情况。通过荧光实时定量PCR法检测LOX-1、VCAM-1、ICAM-1mRNA的表达水平。结果 ox-LDL可以抑制SVAREC细胞的增殖,并呈剂量依赖性,与对照组比较有统计学意义(P<0.05)。ox-LDL+Ang(1-7)组可以使SVAREC细胞生长抑制率降低,并呈剂量依赖性,与对照组比较有统计学意义(P<0.05)。随着ox-LDL浓度的升高,LOX-1、ICAM-1及VCAM-1 mRNA表达量上升,并呈剂量依赖性,与对照组比较有统计学意义(P<0.05),加入Ang(1-7),随着Ang(1-7)的浓度升高,LOX-1、ICAM-1及VCAM-1mRNA表达量下降。结论 ox-LDL可以损伤SVAREC细胞,并使LOX-1、ICAM-1及VCAM-1mRNA表达量上升,Ang(1-7)抑制ox-LDL的上述反应,并且可能通过LOX-1、ICAM-1及VCAM-1mRNA发挥作用。 Objective To investigate the effect of angiotensin (1-7) [Ang (1-7)] on oxidative low density lipoprotein (ox-LDL) induced rat aortic endothelial cells (SVAREC) hemagglutinin-like oxidized low density lipoprotein (LOX-1), intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) Methods The rats were randomly divided into ox-LDL group and ox-LDL + Ang group (1-7). Cell proliferation was detected by Cell Counting Kit-8 (CCK-8 for short). The expression levels of LOX-1, VCAM-1 and ICAM-1 mRNA were detected by real-time fluorescence quantitative PCR. Results ox-LDL could inhibit the proliferation of SVAREC cells in a dose-dependent manner, which was statistically significant compared with the control group (P <0.05). Compared with control group, ox-LDL + Ang (1-7) group could reduce the growth inhibition rate of SVAREC cells in a dose-dependent manner (P <0.05). The mRNA expression of LOX-1, ICAM-1 and VCAM-1 increased with the increase of ox-LDL concentration in a dose-dependent manner. Compared with the control group, the mRNA expression of LOX- -7). The mRNA expression of LOX-1, ICAM-1 and VCAM-1 decreased with the increase of Ang (1-7) concentration. Conclusion Ox-LDL can damage SVAREC cells and increase the expression of LOX-1, ICAM-1 and VCAM-1 mRNA. Ang (1-7) inhibits the above reaction of ox-LDL, And VCAM-1 mRNA play a role.
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