【摘要】 目的探讨Toll样受体4(TLR4)在血管紧张素Ⅱ(AngⅡ)所致高血压小鼠血管重构中的作用。方法选择野生型C57小鼠18只,随机分为对照组、AngⅡ组和TLR4组,每组6只。AngⅡ灌注7d,于灌泵前2d至灌泵后7d小鼠尾静脉注射TLR4中和抗体。免疫组织化学检测胸主动脉内皮素1、增殖细胞核抗原(PCNA)、α-平滑肌肌动蛋白(α-SMA)、细胞间黏附分子1(ICAM-1)的表达;流式细胞仪检测T细胞表面活化分子CD69的表达。结果与对照组比较,AngⅡ组小鼠血压、内皮素1、PCNA、ICAM-1、CD69表达明显上调,α-SMA表达明显下调(P<0.05,P<0.01)。与AngⅡ组比较,TLR4组小鼠血压、内皮素1、PCNA、ICAM-1、CD69表达明显下调,α-SMA表达明显上调(P<0.05,P<0.01)。结论 TLR4通过介导炎性反应参与AngⅡ所致高血压小鼠血管重构。更多还原

【Abstract】 Objective To study the role of TLR4 in angiotension Ⅱ(AngⅡ)-induced vascular remodeling of hypertensive mice.Methods Eighteen wild C57 mice were divided into control group,AngⅡgroup and TLR4 group(6 in each group).The mice were infused with AngⅡfor 7 days and injected with TLR4 through the tail vein to neutralize antibodies 2 days before AngⅡinfusion and 7 days after AngⅡinfusion.Expressions of ET-1,α-SMA,PCNA,ICAM-1 and CD69 were detected by immunohistpchemistry and flow cytometry,respectively.Results The blood pressure and expression levels of ET-1,ICAM-1 and CD69 were significantly higher whereas the expression level of α-SMA was significantly lower in AngⅡgroup than in control group(P<0.05,P<0.01).The blood pressure and expression levels of ET-1,PCNA,ICAM-1 and CD69 were significantly lower whereas the expression level of α-SMA was significantly higher in TLR4 group than in AngⅡgroup(P<0.05,P<0.01).Conclusion TLR4 participates in AngⅡ-induced vascular remodeling of hypertensive mice by mediating inflammatory reactions.更多还原