Sodium meta-arsenite prevents the development of autoimmune diabetes in NOD mice
- Authors
- Lee, Y. S.; Kim, D.; Lee, E. K.; Kim, S.; Choi, C. S.; Jun, H. S.
- Issue Date
- 15-Apr-2015
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Sodium meta-arsenite; Type 1 diabetes; Autoimmune; Proliferation; Glut1; Non-obese diabetic mice
- Citation
- TOXICOLOGY AND APPLIED PHARMACOLOGY, v.284, no.2, pp.254 - 261
- Journal Title
- TOXICOLOGY AND APPLIED PHARMACOLOGY
- Volume
- 284
- Number
- 2
- Start Page
- 254
- End Page
- 261
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/10603
- DOI
- 10.1016/j.taap.2014.12.016
- ISSN
- 0041-008X
- Abstract
- Sodium meta-arsenite (SA) is an orally available arsenic compound. We investigated the effects of SA on the development of autoimmune type 1 diabetes. Female non-obese diabetic (NOD) mice were orally intubated with SA (5 mg/kg/day) from 8 weeks of age for 8 weeks. The cumulative incidence of diabetes was monitored until 30 weeks of age, islet histology was examined, and lymphocytes including T cells, B cells, CD4+ IFN-gamma+ cells, CD8+ IFN-gamma+ cells, CD4+ IL-4+ cells, and regulatory T cells were analyzed. We also investigated the diabetogenic ability of splenocytes using an adoptive transfer model and the effect of SA on the proliferation, activation, and expression of glucose transporter 1 (Glut1) in splenocytes treated with SA in vitro and splenocytes isolated from SA-treated mice. SA treatment decreased the incidence of diabetes and delayed disease onset. SA treatment reduced the infiltration of immunocytes in islets, and splenocytes from SA-treated mice showed a reduced ability to transfer diabetes. The number of total splenocytes and T cells and both the number and the proportion of CD4+ IFN-gamma+ and CD8+ IFN-gamma+ T cells in the spleen were significantly reduced in SA-treated NOD mice compared with controls. The number, but not the proportion, of regulatory T cells was decreased in SA-treated NOD mice. Treatment with SA either in vitro or in vivo inhibited proliferation of splenocytes. In addition, the expression of Glut1 and phosphorylated ERK1/2 was decreased by SA treatment. These results suggest that SA reduces proliferation and activation of T cells, thus preventing autoimmune diabetes in NOD mice. (C) 2015 Elsevier Inc. All rights reserved.
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