OBJECTIVE: Diabetes mellitus is one of the chronic metabolic diseases which is characterized by microvascular and macrovascular complications. This study was designed to investigate the improving the effects of amnioguanidine on aortic damage in a streptozotocin (STZ) induced diabetic rat model. METHODS: Thirty-two male Sprague-Dawley rats divided into four groups as follows: Control, Aminoguanidine, Diabetes, and Diabetes+Aminoguanidine. Experimental diabetes was induced by single dose STZ (45 mg/kg) intraperitoneally. After administration of STZ, the DM+AMG group began to receive AMG (1 g/L) was prepared by dissolving in tap water during 10 weeks. At the end of the study, blood glucose levels were determined and rats were sacrified by ketamine anesthesia. Following routine tissue process, aortas were embedded in paraffin. Histochemical (H-E and Orcein) and immunohistochemical α-smooth muscle actin (α-SMA) stains were applied and the sections examined by light microscope. Statistical analysis was carried out using the SPSS 13.0 statistical program. RESULTS: The rats in diabetes group had significantly higher blood glucose levels than the rats of control. The main histological alterations were detected in tunica media such as extensive thickening (414.32±9.62 μm), irregular of elastic fibers and intensive α-SMA staining in diabetic rats. The thickness of tunica media was statistically increased in DM group, when compared with the control group (p<0.001). On the other hand, AMG prevented disorganization of elastic fibers and overexpression of α-SMA. The mean thickness of tunica media was decreased significantly in DM+AMG (319.16±6.53 μm) compared with the DM group (p<0.001). CONCLUSION: Our results demonstrate that AMG treatment may protect the impairment of aort structure at histological level.
OBJECTIVE:Diabetes mellitus is one of the chronic metabolic diseases which is characterized by microvascular and macrovascular complications. This study was designed to investigate the improving the effects of amnioguanidine on aortic damage in a streptozotocin (STZ) induced diabeticrat model. METHODS: Thirty-two male Sprague-Dawley rats divided into four groups as follows: Control, Aminoguanidine, Diabetes, and Diabetes+Aminoguanidine. Experimental diabetes was induced by single dose STZ (45 mg/kg) intraperitoneally. After administration of STZ, the DM+AMG group began to receive AMG (1 g/L) was prepared by dissolving in tap water during 10 weeks. At the end of the study, blood glucose levels were determined and rats were sacrified by ketamine anesthesia. Following routine tissue process, aortas were embedded in paraffin. Histochemical (H-E and Orcein) and immunohistochemical α-smooth muscle actin (α-SMA) stains were applied and the sections examined by light microscope. Statistical analysis was carried out using the SPSS 13.0 statistical program. RESULTS: The rats in diabetes group had significantly higher blood glucose levels than the rats of control. The main histological alterations were detected in tunica media such as extensive thickening (414.32±9.62 μm), irregular of elastic fibers and intensive α-SMA staining in diabeticrats. The thickness of tunica media was statistically increased in DM group, when compared with the control group (p<0.001). On the other hand, AMG prevented disorganization of elastic fibers and overexpression of α-SMA. The mean thickness of tunica media was decreased significantly in DM+AMG (319.16±6.53 μm) compared with the DM group (p<0.001). CONCLUSION: Our results demonstrate that AMG treatment may protect the impairment of aort structure at histological level.