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Diabetes is associated with micro- and macro-vascular complications affecting several organs. Oxidative stress plays a crucial role in the etiology of vascular disease in diabetes.The present study aimed to investigate the beneficial effect of troxerutin on diabetes-induced histopathological damages in rat aorta with focusing on its antioxidative actions.Male Wistar rats were randomly divided into four groups (n = 8/each): control, control plus troxerutin, diabetic and diabetic plus troxerutin. Diabetes was induced in rats by a single intraperitoneal injection of streptozotocin (50 mg/kg) and lasted for 10 weeks. Troxerutin was administered orally in concentration of 150 mg/kg/daily for one month before killing rats. At the end of treatment period, thoracic aorta was isolated and divided into two parts; one part was immersed in 10% formalin for histopathological evaluations and the other was frozen by liquid nitrogen for assessment of malondialdehyde (MDA, the main product of lipid peroxidation), activity of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPX).Lipid deposition in tunica intimae and media, thickening and structural deformity of vascular tissues as well as the level of plasma glucose and aortic tissue levels of lipid peroxidation were significantly increased in diabetic rats compared to control ones (P < 0.05). Troxerutin significantly reduced the severity of all vascular histopathological damages in treated versus untreated diabetic rats. In addition, treatment of diabetic rats with troxerutin significantly decreased the levels of MDA (5.1 ± 0.3 vs. 9.3 ± 1.2 nmol/mL) (P < 0.01) and increased the activity of antioxidant enzyme GPX compared to untreated-diabetic groups.Troxerutin may reduce the vascular complications and tissue injuries induced by chronic diabetes in rat aorta through increasing the activity of tissue antioxidant system and reducing the level of lipid peroxidation.

Beneficial Effect of Troxerutin on Diabetes-Induced Vascular Damages in Rat Aorta: Histopathological Alterations and Antioxidation Mechanism