| Objective: To explore the role of TGF-β1/SMADs alterations in the pathogenesis of diabetic cardiomyopathy in STZ rats and the protection mechanism of rosiglitazone on diabetic heart.Methods: 30 male SD rats were randomly divided into control (C)group,DM(D) group and rosiglitazone(R) group,each had 10 rats.DM rats were induced by a single intraperitoneal injection of streptozotocin (60mg/kg).A cannula connected to a transducer was inserted the heart for the measurement of the cardiac function.The body weight(BW),heart weight(HW) and HW/BW were measured.The ultrastructural changes were evaluated by electron microscope,collagen content was observed by VG staining and myocardial apoptosis was detected by TUNEL.The mRNA expression level of SMAD3 and SMAD7 were determined by RT-PCR. The protein level of TGF-β1,SMAD3 and SMAD7 were detected by immunohistochemistry.Results: Comparing with the control group,diabetic rats experienced markedly myocardium damage:cardiac function,especially diastolic function were impaired,HW/BW (p<0.01) and cardiomyocytes apoptosis index(p<0.01) as well as collagen content (p<0.01) were much higher, Ultrastructural changes,such as myofilament fragmentation,blood capillary basement membrane thickening and interstitial fibrosis were observed.the protein level of TGF-β1 increased greatly,the mRNA expression and protein level of SMAD3 increased significantly and the level of SMAD7 decreased markedly.Conclusions:1.12 weeks after the T1DM were induced, rats showed heart hypertrophy,Interstitial fibrosis and increased cardiac myocytes apoptosis, indicating pathologic alterations of diabetic cardiomyopathy.2.The changes of TGF-β1/SMADs in the diebetic myocardium paralleled with the progression of myocardium damages,indicating that TGF-β1/SMADs may play important role in the pathogenesis of diabetic cardiomyopathy.3.Rosiglitazone can protect the impaired cardiac function and retard the progression of diabetic cardiomyopathy,it may relate with its action on TGF-β1/SMADs.
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