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目的探讨氨基胍抑制DM大鼠心肌间质纤维化的机制及其对心功能的影响。方法雄性SD大鼠30只,随机分成正常对照组(NC)、DM组和氨基胍干预(A)组,每组各10只。采用STZ一次性腹腔注射建立DM动物模型。12周后检测大鼠血清AGEs、左室心肌胶原含量、结缔组织生长因子(CTGF)mRNA和蛋白质表达及血流动力学。结果与NC组相比,DM大鼠血清AGEs的荧光值(7.21±2.2 vs 2.63±0.62,P<0.01)、左室心肌组织胶原含量(16±3%vs 12±2%,P<0.01)及CTG-FmRNA和蛋白质表达水平(0.077±0.0037 vs 0.0102±0.0034,0.51±0.01 vs 0.34±0.02,P<0.01)均明显升高,心功能明显减低;应用氨基胍干预后上述异常明显减轻。结论氨基胍通过抑制AGEs的形成及心肌组织的CTGF的表达来逆转DM大鼠心肌间质纤维化并改善心脏功能。
Objective To investigate the mechanism of aminoguanidine in inhibiting myocardial interstitial fibrosis in DM rats and its effect on cardiac function. Methods Thirty male SD rats were randomly divided into normal control group (NC), DM group and aminoguanidine intervention group (A), with 10 rats in each group. DM animal model was established by intraperitoneal injection of STZ. After 12 weeks, serum AGEs, collagen content in left ventricular myocardium, CTGF mRNA and protein expression and hemodynamics were detected. Results Compared with NC group, the serum levels of AGEs in DM rats were significantly lower than those in NC rats (7.21 ± 2.2 vs 2.63 ± 0.62, P <0.01), and collagen content in left ventricular myocardium (16 ± 3% vs 12 ± 2%, P <0.01) (0.077 ± 0.0037 vs 0.0102 ± 0.0034, 0.51 ± 0.01 vs 0.34 ± 0.02, P <0.01), and the cardiac function was significantly decreased. The above abnormalities were relieved after treatment with aminoguanidine. Conclusion Aminoguanidine can reverse myocardial fibrosis and improve cardiac function in DM rats by inhibiting the formation of AGEs and the expression of CTGF in myocardium.