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目的探讨血管紧张素Ⅱ(AngⅡ)对人脐静脉内皮细胞分泌单核细胞趋化因子-1 (MCP-1)的影响,以及激活过氧化物酶增殖物激活受体(PPARs)中α、γ亚型对MCP-1的影响。方法以RT-PCR和ELISA方法测定AngⅡ在不同浓度(10-8-10-6 mol/L)对人脐静脉内皮分泌MCP-1的影响以及血管紧张素Ⅱ1型受体(AT1R)拮抗剂缬沙坦的干预作用;同时分析PPARα配体非诺贝特及PPARγ配体罗格列酮的干预对AngⅡ诱导MCP-1表达的效应。结果AngⅡ显著刺激人脐静脉内皮细胞系(HUVEC-12)表达MCP-1,增加的程度与AngⅡ的浓度呈正相关,罗格列酮和非诺贝特均可呈浓度依赖的抑制HUVEC-12中由AngⅡ所诱导的MCP-1的表达。结论AngⅡ可刺激HUVEC-12细胞表达MCP-1,其作用与AT1R受体相关;激动剂PPARα、PPARγ均可明显抑制AngⅡ所诱导的内皮细胞中MCP-1表达。
Objective To investigate the effects of angiotensin Ⅱ on the secretion of monocyte chemoattractant protein-1 (MCP-1) from human umbilical vein endothelial cells and the effects of α, γ on activation of peroxisome proliferator activated receptor (PPARs) Effect of subtypes on MCP-1. Methods The effects of Ang Ⅱ on the secretion of MCP-1 by human umbilical vein endothelial cells (VECs) at different concentrations (10-8-10-6 mol / L) and the effects of angiotensin Ⅱ type 1 receptor (AT1R) antagonist valine Sartan. Meanwhile, the effects of PPARα ligand fenofibrate and PPARγ ligand rosiglitazone on the expression of MCP-1 induced by AngⅡwere analyzed. Results AngⅡ significantly stimulated the expression of MCP-1 in human umbilical vein endothelial cell line (HUVEC-12), and the increase was positively correlated with the concentration of AngⅡ. Both rosiglitazone and fenofibrate inhibited the expression of MCP-1 in HUVEC-12 The expression of MCP-1 induced by Ang II. Conclusions AngⅡ can stimulate the expression of MCP-1 in HUVEC-12 cells, which is related to AT1R receptor. The agonists PPARα and PPARγ can significantly inhibit the expression of MCP-1 in endothelial cells induced by AngⅡ.