Objective: To investigate the effect of diabetes on the expression of transforming growth factor-β1(TGF-β1)

transforming growth factor-β receptors Ⅱ antibodies(TGF-β RⅡ) and signal transduction molecules 7(Smad7) in rats myocardium and the intervention effects of Didang Tang and its split recipes. Method: The 12 healthy male SD rats were chosen randomly as normal group

and other 105 SD male rats were injected intraperitoneally with STZ to induce diabetes(DM) rat models

which were randomized into model group

Didang Tang group

leech and mang worm group

peach kernel and rheum officinale group

and valsartan group

receiving corresponding intervention. At the end of 8-week treatment

fasting blood glucose(FBG) was detected by full-automatic biochemical analyzer

pathomorphological change of myocardium was observed through hematoxylin-eosin staining

and the protein expression of TGF-β1

TGF-β RⅡ and Smad7 were assessed by Western blot. Result: Compared with the normal group

cell hypertrophy was observed in myocardial tissues

with obvious infiltration of inflammatory cells

significant increase in TGF-β1

TGF-β RⅡexpression and significant decrease in Smad7 expression(P<0.01). Compared with the model group

Didang Tang could significantly down-regulate TGF-β1 and TGF-β RⅡexpression and significantly down-regulate Smad7 expression(P<0.05

P<0.01). Compared with the diabetic rat models

the split recipe groups could down-regulate TGF-β1 expression and improve myocardial damages

but the effect was inferior to that of whole prescription group. Conclusion: Didang Tang could relieve cardiac fibrosis of diabetic rats and its mechanism may be associated with down-regulating TGF-β1 and TGF-β RⅡexpression in myocardium of diabetic rats and up-regulating Smad7 expression. In addition

the prophylactic and therapeutic effect of Didang Tang was better than that of its split recipes.The treatment of 'expelling heat

removing blood stasis and dredging collaterals' was associated with inhibiting TGF-β1/Smad7 signal transduction pathway.