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。
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, a-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 a-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 ,PCNA,ICAM-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.
出处
《中华老年心脑血管病杂志》
CAS
北大核心
2013年第1期67-70,共4页
Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
基金
国家自然科学基金(81170269)
