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目的:观察福辛普利对糖尿病大鼠心功能、心肌局部血管紧张素Ⅱ(AngⅡ)浓度及转化生长因子(TGF-β1)表达的影响。探讨福辛普利通过AngⅡ和TGF-β1保护心功能的机制。方法:30只SD大鼠,随机取20只大鼠建立糖尿病模型后,再随机分为福辛普利治疗组(干预组)及糖尿病未治疗组(未治疗组),每组10只,另10只作为正常对照组。治疗组以福辛普利15 mg/(kg.d)水溶液灌胃,对照组和未治疗组每天以同等体积清水灌胃。9周后,用超声心动图观察心功能,放射免疫法测定心肌局部AngⅡ的水平,用免疫组织化学法检测心肌细胞中TGF-β1的表达含量。结果:糖尿病未治疗组心肌局部AngⅡ含量显著高于正常对照组(5 367.43±498.28和4 340.67±348.37,P<0.01),福辛普利干预组AngⅡ含量显著降低(4 501.50±129.33,P<0.01)。未治疗组心肌局部的TGF-β1表达显著高于对照组(0.266 5±0.049 3和0.135 2±0.050 7,P<0.01);福辛普利干预后TGF-β1表达则明显降低(0.140 9±0.039 6,P<0.01)。未治疗组心功能明显低于对照组(P<0.01);福辛普利干预组心功能显著改善(P<0.01)。相关分析表明:未治疗组心肌局部AngⅡ含量与心肌TGF-β1表达明显正相关(r=0.802,P<0.05);而AngⅡ的含量和TGF-β1的表达分别与心功能明显负相关(r=-0.832P<0.05,r=-0.776,P<0.05)。结论:福辛普利能通过降低心肌局部AngⅡ含量而减少心肌TGF-β1表达,减轻心功能的恶化。
Objective: To observe the effects of fosinopril on cardiac function, myocardial angiotensin Ⅱ (Ang Ⅱ) concentration and the expression of transforming growth factor (TGF-β1) in diabetic rats. To investigate the mechanism of Fosinopril in protecting cardiac function by AngⅡ and TGF-β1. Methods: Thirty SD rats were randomly divided into two groups: 20 rats in each group, and then randomly divided into fosinopril treatment group (intervention group) and diabetic untreated group (untreated group), with 10 rats in each group. 10 as a normal control group. The treatment group was orally administered with fosinopril 15 mg / (kg.d) aqueous solution, while the control group and the untreated group were orally administered with the same volume of water daily. After 9 weeks, the cardiac function was observed by echocardiography. The level of AngⅡ in myocardium was measured by radioimmunoassay. The expression of TGF-β1 in myocardial cells was detected by immunohistochemistry. Results: Compared with normal control group, the content of AngⅡ in myocardium of diabetic untreated group was significantly higher than that of normal control group (5 367.43 ± 498.28 and 4340.67 ± 348.37, P <0.01), while the levels of Ang Ⅱ in fosinopril group were significantly decreased (4 501.50 ± 129.33, P < 0.01). The expression of TGF-β1 in untreated myocardium was significantly higher than that in control group (0.266 5 ± 0.049 3 and 0.135 2 ± 0.050 7, P <0.01), while the expression of TGF-β1 was significantly decreased after fosinopril treatment (0.140 9 ± 0.039 6, P <0.01). The cardiac function of the untreated group was significantly lower than that of the control group (P <0.01). The cardiac function of the fosinopril group was significantly improved (P <0.01). Correlation analysis showed that there was a significant positive correlation between myocardial AngⅡ content and myocardial TGF-β1 expression in untreated group (r = 0.802, P <0.05), while AngⅡ content and TGF-β1 expression were negatively correlated with cardiac function (r = -0.832P <0.05, r = -0.776, P <0.05). CONCLUSION: Fosinopril can decrease the expression of TGF-β1 in myocardium and decrease the deterioration of cardiac function by decreasing the content of AngⅡ in myocardium.