Objective To study the role of TLR4 in angiotension Ⅱ (Ang Ⅱ )-induced vascular remodeling of hypertensive mice . Methods Eighteen wild C57 mice were divided into control group ,Ang Ⅱ group and TLR4 group(6 in each group). The mice were infused with Ang Ⅱ for 7 days and injected with TLR4 through the tail vein to neutralize antibodies 2 days before Ang Ⅱ infusion and 7 days after Ang Ⅱ infusion .Expressions of ET-1 ,α-SM A ,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 Ang Ⅱ group than in control group (P<0. 05 , P<0 .01) .The blood pressure and expression levels of ET -1 ,PCN A ,IC AM-1 and CD69 were significantly lower whereas the expression level of a-SMA was significantly higher in TLR4 group than in Ang Ⅱ group(P<0 .05 , P<0 .01) .Conclusion TLR4 participates in Ang Ⅱ-induced vascular remodeling of hypertensive mice by mediating inflammatory reactions .%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7 d,于灌泵前2 d至灌泵后7 d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.
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