RESUMEN
<p><b>OBJECTIVE</b>To study the protective effect of the Mixture of Shengmai Powder and Danshen Decoction (, abbreviated as the Mixture) in the rat model with type 2 diabetic cardiomyopathy in the rat model with type 2 diabetic cardiomyopathy, abbreviated as the Mixture) in the rat model with type 2 diabetic cardiomyopathy (DCM).</p><p><b>METHODS</b>Forty-two SD rats with DCM model, established by the combination of insulin resistance by a high-fat diet with the damage of pancreatic islet β cells by intraperitoneal injection of high dose streptozotocin (50 mg/kg) once, were evaluated in the damage of the myocardium by electrocardiogram at the end of 12 weeks of grouping and intervention administration; the extent of damage in the myocardial subcellular structure was observed by electron microscopy; the content of myocardial collagen in the left cardiac ventricle was quantified by Masson staining test; the myocardial cell apoptosis was determined by TUNEL; the changes in the mRNA expression levels of thrombospodin-1 (TSP-1) and tribbles homolog 3 (TRB-3) by real-time quantitative PCR, the expression levels of myocardial TSP-1, tumor growth factorβ1 (TGF-β1), TRB-3, and chymase were detected by immunohistochemistry, and the changes in the expression levels of myocardial TSP-1, active-TGF-β1 (A-TGF-β1) and latent-TGF-β1 (L-TGF-β1) protein were tested by Western blotting.</p><p><b>RESULTS</b>Compared with the control group, the myocardial tissue was less damaged, and the extent of damage in the myocardial subcellular structure was less; the collagen fiber content and the cell apoptosis were reduced; the expression levels of TSP-1mRNA and TRB-3 mRNA, the expression levels of myocardial TSP-1, TGF-β1, TRB-3, and chymase, as well as the average expression levels of the myocardial TSP-1, A-TGFβ1, and L-TGF-β1 protein were decreased in the Mixture group.</p><p><b>CONCLUSION</b>The Mixture of Shengmai Powder and Danshen Decoction could inhibit the process of myocardial fibrosis in the rat myocardium of DCM through multiple pathways and significantly delay the genesis and progress of DCM in hyperglycemic rats.</p>