Selenium Downregulates RAGE and NFκB Expression in Diabetic Rats

Abstract

Diabetes is one of the leading causes of death in developed and developing countries. Oxidative stress has been proposed to play a crucial role in the pathogenesis of diabetic vascular complications. In recent years, selenium has been shown to mediate a number of insulinlike actions in a dose-dependent fashion both in vitro and in vivo. In this study, the effect of selenium as sodium selenite was investigated in streptozotocin-induced diabetic rats at the dose of 1 μg sodium selenite/kg body weight. Selenium supplementation restored the streptozotocin-induced alterations in the activities of antioxidant enzymes, decreased the serum glucose level, glycated hemoglobin content as well as the levels of lipid peroxidation products, and downregulated the expressions of both NFkB and RAGE. The histopathological studies also reinforce our findings. Hence, selenium has a protective role in streptozotocin-induced diabetes mellitus.

Hyperoside Downregulates the Receptor for Advanced Glycation End Products (RAGE) and Promotes Proliferation in ECV304 Cells via the c-Jun N-Terminal Kinases (JNK) Pathway Following Stimulation by Advanced Glycation End-Products In Vitro

“…These include antihypertensive drugs (Telmisartan [14] and Candesartan [15]), vitamin A [16], selenium [17], n-3 polyunsaturated fatty acids [18], antihyperlipidemic agents (statins) [19], antidiabetic agents (thiazolidinediones) [20], peroxisome proliferator-activated receptor gamma [21] and several extracts from Chinese traditional medicines, such as ginkgo biloba extract [22] and Panax notoginseng saponins (PNS) [23]. This suggests that reduced expression of RAGE may contribute to the therapeutic value of these drugs.…”

The Pharmacology and Biochemistry of Selenium in Cancer

“…Several pathways have been proposed that could explain how selenium-containing compounds could block mutated cells from progressing to cancer. Methylseleninic acid has been shown to inhibit NF-kappa B and regulate I kappa B in prostate cancer cells [68]. Selenium compounds inhibit signaling enzymes such as protein kinase C (PKC) [66] that play crucial roles in tumor promotion.…”

Sodium selenite ameliorates dextran sulfate sodium-induced chronic colitis in mice by decreasing Th1, Th17, and γδT and increasing CD4(+)CD25(+) regulatory T-cell responses

“…Activation of NF-κB and AP-1 is important in the pathogenesis of IBD[19,20]. Although Se has been shown to affect NF-κB and AP-1 activation[21-24], the effect of Se on mucosal LPL in the colon remains unclear.…”