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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。
The aim of this study was to investigate the effect of β-CM7 on Renin angiotensin system (RAS) and its protective mechanism in diabetic rats. 32 male Sprague-Dawley rats were divided into normal control group, model control group, insulin treatment group (3.7 × 10 -8 mol / d) and β-CM7 intervention group (7.5 × 10 -8 ) mol / d). After continuous feeding for 30 days, the rats were sacrificed to take the myocardium. After intervention with β-CM7, the content of AngⅡ and the content of Ang1-7 were significantly decreased. The mRNA expression of AT1 receptor and Mas receptor were significantly increased. The mRNA and protein expressions of ACE and ACE2 were significantly increased, And enzyme activity were significantly increased. In summary, β-CM7 can significantly inhibit the myocardial ACE mRNA and protein expression, attenuate Ang Ⅱ myocardial injury by activating the negative regulatory pathway of “RAS” “ACE2-Ang1-7-Mas axis” It is suggested that the effect of β-CM7 on myocardial injury may be related to ACE / ACE2 pathway.