Toll样受体2在血管紧张素Ⅱ致高血压小鼠心肌纤维化中的作用

摘要

Objective To study the role of TLR2 in AngⅡ-induced cardiac fibrosis in hypertensive mice .Methods Eighteen wild C57 mice were randomly divided into blank control group ,AngⅡgroup and TLR2 blocking group (6 in each group) .A hypertension model was established by sub-cutaneous infusion of AngⅡthrough a mini-pump for 7 days .Cardiac fibrosis in mice was observed with immunohistochemical staining .Results The area of cardiac fibrosis was significantly larger and the expression levels of collagen Ⅰ and TGF-βwere significantly higher in Ang Ⅱgroup than in blank control group (P<0 .05) .The area of cardiac fibrosis was 71 .2% smaller ,the expression level of collagen Ⅰ was 75 .5% ,and the expression level of TLR2 was 77 .7% lower in TLR2 blocking group than in Ang Ⅱgroup (P<0 .05) .Conclusion TLR2 is involved in Ang Ⅱ-induced cardiac fibrosis in hypertensive mice .%目的：探讨Toll样受体（TLR）2在血管紧张素Ⅱ（AngⅡ）所致高血压小鼠心肌纤维化过程中的作用。方法选择SPF级雄性野生型C57小鼠18只，随机分为对照组、AngⅡ组和TLR2阻断组，每组6只。AngⅡ组和TLR2阻断组采用皮下微量泵持续灌注AngⅡ7 d建立高血压模型，小鼠尾动脉套法测血压。TLR2阻断组尾静脉注射TLR2中和抗体后，Masson染色、免疫组织化学染色观察心肌纤维化。结果与对照组比较，AngⅡ组小鼠心肌纤维化明显升高，心肌间质有大量胶原纤维，Ⅰ型胶原蛋白和转化生长因子β蛋白表达显著升高，差异有统计学意义（P＜0．05）；与AngⅡ组比较，TLR2阻断组小鼠心肌间质纤维化面积减少71．2％，Ⅰ型胶原蛋白表达减少75.5％，转化生长因子β蛋白表达下降77．7％，差异有统计学意义（P＜0．05）。结论 TLR2参与AngⅡ所致高血压小鼠心脏纤维化过程。