Oxidative Stress-Induced Sirtuin1 Downregulation Correlates to HIF-1α, GLUT-1, and VEGF-A Upregulation in Th1 Autoimmune Hashimoto’s Thyroiditis

In Hashimoto’s thyroiditis (HT), oxidative stress (OS) is driven by Th1 cytokines’ response interfering with the normal function of thyrocytes. OS results from an imbalance between excessive production reactive oxygen species (ROS) and a lowering antioxidant production. Moreover, has been shown to inhibit Sirtuin 1 (SIRT1), which able prevent hypoxia-inducible factor (HIF)-1α stabilization. The aims this study were determine involvement NADPH-oxidases (NOX), SIRT1, HIF-1α in HT pathophysiology as well status proteins such peroxiredoxin (PRDX1), catalase, superoxide dismutase (SOD1). protein expressions NOX2, NOX4, enzymes, HIF-1α, glucose transporter-1 (GLUT-1) vascular endothelial growth A (VEGF-A), analyzed Western blot primary cultures human thyrocytes that or not incubated cytokines. same also immunohistochemistry thyroid samples control patients. cytokines, NOX4 expression was increased whereas antioxidants, PRDX1, SOD1, reduced. cytokines induced significant decrease SIRT1 associated upregulation GLUT-1, VEGF-A proteins. With exception PRDX1 similar obtained thyroids. due increase ROS produced loss defenses (PRDX1, SOD1) correlates reduction HIF 1α, VEGF-A. Our placed key regulator we, therefore, believe it could be considered potential therapeutic target HT.