【摘要】 目的探讨Toll样受体4(TLR4)在血管紧张素Ⅱ(AngⅡ)所致高血压小鼠心脏纤维化过程中的作用。方法野生型C57小鼠18只分为3组:空白对照组、AngⅡ组和TLR4阻断组,每组6只。AngⅡ组和TLR4阻断组AngⅡ微量泵灌注建立高血压模型,TLR4阻断组尾静脉注射TLR4中和抗体后,小鼠尾动脉套法测血压,心动超声图观察小鼠的心脏功能变化。免疫组织化学、Masson染色观察心脏纤维化。RT-PCR检测心肌白细胞介素1β和单核细胞趋化蛋白1 mRNA表达。结果与AngⅡ组比较,TLR4阻断组小鼠血压降低,左心室舒张末期壁厚度减少,舒缩未期左心室内径增加(P<0.05)。心肌组织半乳糖凝集素2阳性巨噬细胞浸润减少,白细胞介素1β和单核细胞趋化蛋白1 mRNA表达水平降低(P<0.05)。小鼠心肌间质和血管周围纤维化减轻(P<0.05)。结论 TLR4通过介导炎性反应参与AngⅡ所致高血压小鼠心脏纤维化过程。更多还原

【Abstract】 Objective To study the role of TLR4 in angiotension II(Ang II )-induced cardiac fibrosis in hypertensive mice.Methods Eighteen male wild-type mice were divided into blank control group,Ang II group,and TLR4 blocking group(6 in each group).A hypertension model was established by Ang II perfusion with a micropump.Blood pressure was measured in mice through the tail artey cuff and heart function of the mice was tested by echocardiacgraphy after injection of TLR4 neutralizing antibodies through the tail artery.Cardiac fibrosis in the mice was observed with immunohistochemical and Masson staining.Expressions of myocardial interleukin 1(3 and mononuclear cell chemotactic protein 1 mRNA were detected by RT-PCR.Results The blood pressure was lower,the left ventricular wall was thinner,the inner diameter of left ventricule at the end-diastolic phase was larger,the number of infiltated Mac-2 positive macrphygocytes was less,the expression level of interleukin 1βand mononuclear cell chemotactic protein 1 mRNA was lower,and the fibrosis of myocardial interstitium and peripheral blood vessels was milder in TLR4 blocking group than in Ang U group(P<0.05).Conclusion TLR4 participates in Ang II -induced cardiac fibrosis in hypertensive mice by mediating inflammatory reactions.更多还原