This reduction can contribute to insulin resistance through the inhibition of insulin-stimulated glucose uptake in skeletal muscle, which is actually mediated by increasing blood flow through a NO-dependent pathway. Moreover, reduced production of endothelial NO cause the vascular smooth muscle cells to become more sensitive to the effects of vasoconstrictors, which can result in Dapagliflozin ((2S)-1,2-propanediol, hydrate) increased vascular tone and elevated blood pressure. In this regard, our histopathological findings showed that the aortic sections from rats administered fructose lost some of its elasticity as shown by the relative straightening of elastic fibers in tunica media compared to the control rats. Another important causative factor that might be involved in the progression of fructose-induced impairment of vascular endothelium associated with insulin resistance is oxidative stress. The results of the present study demonstrate that fructose consumption increased oxidative stress in aortic tissues as evidenced by the increased production of MDA, GSH and increased expression of iNOS. Our results are in Cefadroxil agreement with previous reports. Although increased expression of iNOS can result in increased production of NO in aortic tissues, however, under conditions of oxidative stress, superoxide radical is produced which then can interact with NO. This interaction can result in the degradation of NO and the formation of peroxynitrite, a highly toxic oxidant to the vascular tissues. Two main sources of ROS in vascular tissues have been described, namely NADPH oxidase and XO. Indeed, our results showed that the expression of XO in aortic rings from FDR was significantly higher compared to the control rats serving as a continued source of ROS production. In addition, we detected significant leukocyte infiltration in the tunica adventitia of aortic rings from FDR during the histopathological examination. These inflammatory cells play an important role in the consequent vascular dysfunction through increasing the production of ROS primarily by stimulating NADPH oxidase within the vasculature.