Effect of thymoquinon on vascular damage caused by streptozotocin-induced TYPE-1 diabetes

Effect of thymoquinon on vascular damage caused by streptozotocin-induced type-1 diabetes Diabetes is a chronic metabolism disorder with increasing prevalence worldwide. The most complication of diabetes is endothelial dysfunction. Thymoquinone (TQ) has many beneficial effects such as antioxidant, anticancerogenic, antihyperlipidemic, antidiabetic, antiinflamatuar, gastroprotective, hepatoprotective. The aim of this study is to investigate the vascular effects of TQ in STZ-induced diabet model. STZ was injected intraperitoneally at a single dose of 50 mg/kg to induce diabetes. The rats in TQ treated groups were given TQ (80 mg/kg body weight) once a day orally by using intragastric intubation for 3 weeks starting 3 days after STZ injection. Blood pressure of rats (systolic blood pressure) were performed by the indirect tail cuff method from the queue of rat at initial and end of experiment. Blood and thorasic aorta samples were obtained for biochemical, histopathological and pharmacological investigation. Blood pressure was not different between groups control, STZ and STZ+TQ (102.56±4.31, 103.20±5.74, 105.20±2.09 respectively). At isolated rat thoracic aorta, there is no difference between relaxation dose-response curve for Ach after application of submaximal dose of Phe. TQ significantly reduced to phe EC50 values compared to the control group (Control, STZ, STZ+TQ groups respectively; 6.91±0.18, 6.88±0.22, 6.54±0.22). It was determined that there was no significant change in eNOS immunoreactivity between the groups (Control, STZ, STZ+TQ groups respectively; 0.28±0.09, 0.31±0.07, 0.26±0.05). At the third day after application of STZ, blood glucose in STZ-treated group increased significantly (Control, STZ, STZ+TQ groups respectively; 119.50±7.88, 388.25±49.59, 398.11±65.16). At the end of three weeks, only glucose levels were significantly increased compared to baseline in the group STZ (Control, STZ, STZ+TQ groups respectively; 100.20±11.05, 480.50±62.80, 412.20±51.50). In Thoracic aorta, STZ and STZ + TQ applications has reduced significantly the levels of MMP-9 enzyme (Control, STZ, STZ+TQ groups respectively; 15.47±3.80, 2.63±2.13, 3.30±0.73). It was determined that STZ application causes to increase level of CD34 which could prevent by adding of TQ (Control, STZ, STZ+TQ groups respectively; 0.13± 0.05, 1.75± 0.55, 0.15±0.05). According to available evidence, TQ may cause to reducing effect on contraction sensitivity without affecting the Enos activity and relaxation response to acetylcholine in STZ-induced diabet model. In addition, in this model, it may be suggest that TQ has preventive effects on progressive increases of blood glucose without involving the MMP-9 enzyme which may involve the progenitor cell markers CD34 that thought to be associated with a process. Keywords: CD34, diabetes, MMP-9, STZ, thymoquinone