Effect of selenium on pancreatic proinflammatory cytokines in streptozotocin-induced diabetic mice.

To investigate the effects of selenium on mRNA expressions of proinflammatory cytokines and inducible nitric oxide synthase (iNOS) in the pancreas of streptozotocin-induced diabetic mice, the animals were divided into three groups in this study: a normal control group, an untreated diabetes mellitus group and a selenite-treated diabetes mellitus group. Selenite was administered to the diabetic mice in selenite-treated diabetes mellitus group for 2 weeks with an oral dose of 2 mg/kg body weight per day by gavage. The results showed that pancreatic selenium content and glutathione peroxidase mRNA expression and activity were decreased by 16.0%, 63.9% (P<.01) and 31.2 % (P<.01), respectively, in untreated diabetes mellitus group compared with normal control group, and they were significantly increased by 51.0% (P<.001), 79.7% (P<.05) and 21.0% (P<.05), respectively, in selenite-treated diabetes mellitus group compared with untreated diabetes mellitus group. Meanwhile, pancreatic mRNA expressions of proinflammatory cytokines interleukin-1β, tumor necrosis factor-α and interferon-gamma; mRNA expression and activity of iNOS and content of nitric oxide were significantly increased by 133.0% (P<.01), 164.0% (P<.001), 111.0% (P<.01), 101.0% (P<.001), 73.2% (P<.001) and 37.6% (P<.01), respectively, in untreated diabetes mellitus group compared with normal control group, and they were decreased by 43.2% (P<.01), 37.5% (P<.01), 33.9 % (P<.05), 35.5% (P<.01), 34.9% (P<.01) and 18.1% (P<.05), respectively, in selenite-treated diabetes mellitus group compared with untreated diabetes mellitus group. In conclusion, the chosen pharmacological dose of selenium provides partial correction of these effects towards control values. Moreover, the results suggested that the hypoglycemic role of selenium may relate with its inhibiting effect on augmentation of proinflammatory cytokines and reactive oxygen species/reactive nitrogen species by streptozotocin inducing in the pancreas of diabetic mice.