| dc.description.abstract | Objective: Diabetes is associated with vascular complications and impaired angiogenesis. Since angiogenesis plays a crucial role in vascular homeostasis in ischemic heart diseases, in this study, the effect of IMOD (TM) on miR-503 and CDC25 expression level which are altered in impaired angiogenesis were investigated in heart tissue of diabetic rats. Materials and Methods: Forty male Wistar rats (200-250 g) were randomly classified into 4 groups: control (C), IMOD (TM) (I), diabetes (D), and diabetes+IMOD (TM) (D+I). For induction of experimental diabetes in animals, a single dose of streptozotocin (STZ; 60mg/kg) was injected intraperitoneally. After 8 weeks of treatment with IMOD (TM) (20 mg/kg/day), heart tissue samples were removed and used for measurement of miR-503 and CDC25 expression level as well as histological studies. Results: Results of this study showed that diabetes decreased heart tissue angiogenesis which was associated with increased miR-503 and reduced CDC25 expression levels (p<0.05) and IMOD (TM) could reduce the expression of miR-503 and increase the expression of CDC25 (p<0.05). Moreover, IMOD (TM) extensively induced angiogenesis in the heart tissue of diabetic group. However, IMOD (TM) had no significant effect on expressions of miR-503 and CDC25, or angiogenesis in healthy rats. Conclusion: This study showed that IMOD (TM) is able to increase angiogenesis in the heart tissue of diabetic rats. The angiogenic effect of IMOD (TM) is associated with reduction of miR-503 expression and increased expression of CDC25. | |
