β-CM7干预对糖尿病大鼠心肌肾素-血管紧张素系统的影响及其保护机制

Protective effect and mechanism of β-CM7 on renin angiotensin system & diabetic cardiomyopathy

摘要:

本文旨在探究β-CM7对糖尿病大鼠心肌组织肾素-血管紧张素系统 (Renin angiotensin system, RAS) 的影响及其保护机制。32只雄性SD大鼠通过相应处理被分为正常对照组、模型对照组、胰岛素治疗组 (3.7×10–8 mol/d) 及β-CM7干预组 (7.5×10–8 mol/d)。连续饲养30 d后，处死大鼠取心肌。β-CM7在干预糖尿病模型后，组织中AngⅡ含量显著降低，Ang1-7含量极显著升高；AT1受体和Mas受体mRNA表达均显著升高；ACE和ACE2的mRNA表达均显著升高，且酶活均显著升高。综上可得，β-CM7可以通过激活RAS的负性调节通路“ACE2-Ang1-7-Mas轴” 显著抑制大鼠心肌ACE mRNA和蛋白的强表达，缓解AngⅡ对心肌组织的损伤，提示β-CM7抑制心肌损伤的作用可能与ACE/ACE2通路有关。

Abstract:

This article aimed at exploring the effects and protective mechanism of β-CM7 on renin angiotensin system (RAS) in diabetic rats myocardial tissue. We divided 32 male SD rats into 4 groups: control group, diabetic model control group, insulin (3.7×10–8 mol/d) treatment group and β-CM7 (7.5×10–8 mol/d) treatment group. After 30 days, all rats were decapitated and myocardical tissues were collected immediately. After injection, β-CM7 could decrease the content of AngⅡ, increase the content of Ang1-7. And β-CM7 could improve the mRNA of AT1 receptor and Mas receptor. β-CM7 also could improve the mRNA of ACE and ACE2, enhance the activity of ACE and ACE2. These data confirmed that β-CM7 could activate ACE2–Ang1-7–Mas axis, negative passage in RAS, to inhibit the expression ACE mRNA and protein in rat myocardium, alleviate the myocardial tissue damage induced by AngⅡ. The effect of β-CM7 on inhibiting myocardium damage might be related to ACE/ACE2 passageway.