Key result
Shengmai San inhibited myocardial fibrosis and reduced myocardial tissue damage, collagen content, and expression of TSP-1, TGF-beta1, and TRB-3 in a rat model of diabetic cardiomyopathy.
Why the study?
Does Shengmai San protect the myocardium and inhibit fibrosis in a rat model of type 2 diabetic cardiomyopathy?
Does Shengmai San protect the myocardium and inhibit fibrosis in a rat model of type 2 diabetic cardiomyopathy?
Shengmai San demonstrates cardioprotective and anti-fibrotic effects in a rat model of type 2 diabetic cardiomyopathy.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for myocardial protection in diabetic cardiomyopathy; human trials needed before clinical consideration.
OBJECTIVE: To study the effect of Shengmai San ((see text) 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-beta1 (Transforming Growth F factor-beta) and TRB-3 (Tribbles homolog 3) proteins were detected by immunohistochemical method; the expression levels of cardiac TSP-1, A-TGF-beta1 and L-TGF-beta1 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-beta1, TRB-3, and TSP-1, A-TGF-beta1, L-TGF-beta1 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.
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Ni et al. (2011) studied Type 2 diabetic cardiomyopathy (n=42). Shengmai San vs. Model group (untreated DCM rats) and normal group was evaluated on Myocardial damage, collagen content, and expression of TSP-1, TGF-beta1, and TRB-3. Shengmai San inhibited myocardial fibrosis and reduced myocardial tissue damage, collagen content, and expression of TSP-1, TGF-beta1, and TRB-3 in a rat model of diabetic cardiomyopathy.
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