Objective:To study the effect of Shengmai San(生脉散Pulse-activating Powder) in protecting myocardium in the rat of the type 2 diabetic cardiomyopathy(DCM) model.Methods:The DCM rat model was established by combination of insulin resistance induced by a high-fat diet with intraperitoneal injection of high dose streptozotocin(50 mg/kg).And these rat models were randomly divided into three groups:a normal group(n=12,one of them died),a model group(n=15) and a Shengmai San group(treatment group,n=15).The damage of the myocardium was assessed by electrocardiogram at the twelfth week after modeling,and the blood glucose,cholesterol and triglyceride levels were determined;the content of the left cardiac ventricle myocardial collagen was quantified by Masson staining test;the level of myocardial cell apoptosis was detected with TUNEL apoptosis detection kit;the damage extent of the myocardial sub-cellular structures was observed by electron microscopy;the expression levels of cardiac TSP-1(Thrombospondin-1),TGF-β1(Transforming Growth Ffactor-β) and TRB-3(Tribbles homolog 3) proteins were detected by immunohistochemical method;the expression levels of cardiac TSP-1,A-TGF-β1 and L-TGF-β1 proteins were detected by Western blotting;and the expression levels of TSP-1 and TRB-3 mRNAs were detected by real-time quantitative PCR.Results:Compared with the control group,the blood glucose,cholesterol,triglycerides levels in both the model groups and the Shengmai San group were significantly decreased;the myocardial tissue was less damaged and the collagen content was reduced in the Shengmai San group;the myocardial sub-cellular structure was injured to a lesser extent;the expression levels of myocardial TSP-1,TGF-β1,TRB-3,and TSP-1,A-TGF-β1,L-TGF-β1 and chymase were decreased,and the expression levels of TSP-1 mRNA and TRB-3 mRNA were decreased in both the model groups and the Shengmai San group(the latter was better),.Conclusion:Shengmai San can inhibit myocardial fibrosis in the rat of diabetic cardiomyopathy,and significantly delay the formation of diabetic cardiomyopathy in hyperglycemia rats through multiple pathways. Objective: To study the effect of Shengmai San (pulse-activating Powder) in protecting myocardium in the rat of the type 2 diabetic cardiomyopathy (DCM) model. Methods: The DCM rat model was established by combination of insulin resistance induced by a high-fat diet with intraperitoneal injection of high dose streptozotocin (50 mg / kg) .And these rat models were randomly divided into three groups: a normal group (n = 12, one of them died), a model group (n = 15) and a Shengmai San group (treatment group, n = 15). The damage of the myocardium was assessed by electrocardiogram at the twelfth week after modeling, and the blood glucose, cholesterol and triglyceride levels were determined; the content of the left cardiac the level of myocardial cell apoptosis was detected with TUNEL apoptosis detection kit; the damage extent of the myocardial sub-cellular structures was observed by electron microscopy; the expression levels of cardiac TSP-1 Thrombospondin-1, Transforming Growth Ffactor-β and TRB-3 (Tribbles homolog 3) proteins were detected by immunohistochemical method; the expression levels of cardiac TSP-1, A-TGF-β1 and L-TGF -β1 proteins were detected by Western blotting; and the expression levels of TSP-1 and TRB-3 mRNAs were detected by real-time quantitative PCR. Results: Compared with the control group, the blood glucose, cholesterol, triglycerides levels in both the model groups and the Shengmai San group were significantly decreased; the myocardial tissue was less damaged and the collagen content was reduced in the Shengmai San group; the myocardial sub-cellular structure was injured to a lesser extent; the expression levels of myocardial TSP-1 , TGF-β1, TRB-3, and TSP-1, A-TGF-β1, L-TGF-β1 and chymase were decreased, and the expression levels of TSP-1 mRNA and TRB-3 mRNA were decreased in both the model groups and the Shengmai San group (the latter was better). Conclusion: Shengmai San can inhibit myocardial fibrosis in the rat of diabetic cardiomyopathy, and significantly delay the formation of diabetic cardiomyopathy in hyperglycemia rats through multiple pathways.