摘要
目的探讨P-选择素(P-selectin)在血管紧张素Ⅱ诱导的小鼠高血压模型致血管重构中的作用及机制。方法采用P-选择素基因敲除(P-selectin-/-,KO)小鼠,利用血管紧张素Ⅱ微量泵灌注(angiotensinⅡinfusion)构造高血压模型;随机分为4组:WT+PBS组(阴性对照组)、P-selectin-/-+PBS组(空白对照组)、WT+AngⅡ组(阳性对照组)、P-selectin-/-+AngⅡ组(实验组)。免疫组织化学染色观察转化生长因子-β1(TGF-β1)、Smad2/3蛋白在血管的表达水平,RT-PCR法检测血管组织TGF-β1、Smad3基因的表达。结果 WT+AngⅡ组与WT+PBS组、P-selectin-/-+AngⅡ组比较,WT+PBS组与P-selectin-/-+PBS组比较,TGF-β1、Smad3蛋白的表达均升高,其mRNA与其蛋白表达水平基本一致。结论 P-selectin能够上调TGF-β1、Smad3蛋白和mRNA的表达,主要通过加强TGF-β1/Smads信号通路的正反馈路径促进血管重构,AngⅡ发挥协同作用。
Objective To investigate the effect of P - selectin on vascular remodeling induced by angiotensin Ⅱ in mice. Methods P- selectin gene knockout mice,hypertension models were established by micro - pump infusion of angiotensin Ⅱ construct and randomly assigned to 4 groups ： WT ＋PBS group （negative control group）, P - selectin/＋ PBS group （ blank control group）, WT ＋AngⅡ group （positive control group）, and Pselectin/＋ PBS group （experimental group）. The expressions of transforming growth factorbeta 1 （TGF- beta 1） and Smad 2/3 were detected by immunohistochemical staining. The expressions of TGF - beta 1 and Smad 3 gene in vascular were detected by real - time reverse transcription polymerase chain reaction （RT - PCR）. Results WT＋ Ang Ⅱ group compared with WT＋PBS group and Pselectin/＋Ang Ⅱ group, and WT＋PBS group compared with P- selectin/＋ PBS group, the expressions of TGF - beta 1 and Smad 2/3 protein were elevated. The mRNA and its protein expression were at same levels. Conclu- sion P - selectin could upregulate the expression of TGF - beta 1 ,Smad 3 protein and mRNA by strengthening the positive feedback of TGF - beta 1/Smads signal pathway to promote vascular remodeling.
出处
《中西医结合心脑血管病杂志》
2013年第4期452-454,共3页
Chinese Journal of Integrative Medicine on Cardio-Cerebrovascular Disease
基金
国家自然科学基金项目(No.81070090)
