血管紧张素Ⅱ及转化生长因子α在糖尿病心肌病发病机制中的作用

Effect of angiotensin Ⅱ and transforming growth factor α on pathogenesis of diabetic cardiomyopathy

目的探讨血清血管紧张素Ⅱ(angiotensinⅡ,Ang-Ⅱ)及转化生长因子α(transforming growth factorα,TGF-α)浓度在糖尿病(diabetes mellitus,DM)心肌病(diabetic cardiomyopathy,DCM)发病机制中的作用。方法检测118例DCM患者、40例单纯2型DM患者及50名健康体检者(正常对照组)的血清Ang-Ⅱ及TGF-α浓度,并进行对比分析。DCM患者按心功能分级(纽约心脏学会标准)分为3个亚组:35例心功能正常者设为DCM1组,42例心功能Ⅱ级者设为DCM2组,41例心功能Ⅲ～IV级者设为DCM3组。DCM组及DM组血清Ang-Ⅱ及TGF-α浓度进行直线相关分析。结果血清Ang-Ⅱ及TGF-α的浓度在DCM各亚组[Ang-Ⅱ:(99.6±20.3)、(116.9±26.5)、(137.5±33.7)pg/mL;TGF-α:(62.6±9.8)、(75.3±11.2)、(89.3±13.6)pg/mL]及DM组[Ang-Ⅱ:(83.9±17.1)pg/mL;TGF-α:(48.5±8.4)pg/mL]均显著高于正常对照组[Ang-Ⅱ:(56.2±14.4)pg/mL;TGF-α:(26.8±5.1)pg/mL],差异有统计学意义(P均<0.05)。DCM各亚组血清Ang-Ⅱ及TGF-a的浓度均显著高于DM组,差异有统计学意义(P均<0.05)。DCM组及DM组血清Ang-Ⅱ与TGF-α浓度呈正相关(r=0.93,P<0.05;r=0.90,P<0.05)。结论血清Ang-Ⅱ及TGF-α浓度的升高,激活肾素血管紧张素系统,导致心肌纤维化可能是DCM的发病机制之一。

Abstract： Objectives To explore the effect of serum concentrations of angiotensin Ⅱ （Ang-Ⅱ ） and transfbrming growth factor α （TGF-et） on the pathogenesis of diabetic cardiomyopathy （DCM）. Methods Serum concentrations of Ang- Ⅱ and TGF -α were measured, compared and analyzed in 118 patients with DCM, 40 patients with type 2 diabetes mellitus （DM） and 50 normal subjects （control group）. Patients with DCM were divided into 3 subgroups according to New York Heart Association cardiac functional class： 35 patients with normal cardiac function were in DCMI group; 42 patients with cardiac functional class Ⅱ were in DCM2 group,41 patients with cardiac functional class m-IV were in DCM3 group. Linear correlation analysis was carried out between serum concentrations of Ang-II and TGF -α in DCM group and DM group. Results Serum concentrations of Ang-Ⅱ and TGF-α in DCM subgroups [Aug-Ⅱ： （99.6±20.3）, （116.9±26.5）, （137.5±33.7） pg/mL; TGF-α： （62.6±9.8）, （75.3±11.2）, （89.3±13.6） pg/mL] and DM group [Ang-Ⅱ： （83.9±17.1） pg/mL; TGF -ct： （48.5±8.4） pg/mL] were significantly higher than those in control group [Ang-Ⅱ： （56.2±14.4）pg/mL; TGF-α： （26.8±5.1）pg/mL] （/）〈0.05）. Serum concentrations of Ang- Ⅱ and TGF-α in DCM subgroups were significantly higher than those in DM group （P〈0.05）. In DCM group and DM group, serum concentrations of Ang-Ⅱ were significantly positively correlated with serum concentrations of TGF-α （r=0.93,P〈0.05; r=0.90, P〈O.05）. Conclusions The increase in serum concentrations of Ang-Ⅱ and TGF -α activates the renin-angiotensin system, and so induces myocardial fibrosis, which may be one of the pathologiesis of DCM.