Sodium meta-arsenite prevents the development of autoimmune diabetes in NOD mice
DC Field | Value | Language |
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dc.contributor.author | Lee, Y. S. | - |
dc.contributor.author | Kim, D. | - |
dc.contributor.author | Lee, E. K. | - |
dc.contributor.author | Kim, S. | - |
dc.contributor.author | Choi, C. S. | - |
dc.contributor.author | Jun, H. S. | - |
dc.date.available | 2020-02-28T09:44:36Z | - |
dc.date.created | 2020-02-06 | - |
dc.date.issued | 2015-04-15 | - |
dc.identifier.issn | 0041-008X | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/10603 | - |
dc.description.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. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | - |
dc.relation.isPartOf | TOXICOLOGY AND APPLIED PHARMACOLOGY | - |
dc.subject | ACTIVATED T-CELLS | - |
dc.subject | CYTOKINE SECRETION | - |
dc.subject | GENE-EXPRESSION | - |
dc.subject | CANCER-CELLS | - |
dc.subject | PROLIFERATION | - |
dc.subject | LYMPHOCYTES | - |
dc.subject | TRIOXIDE | - |
dc.subject | INVOLVEMENT | - |
dc.subject | DISEASE | - |
dc.subject | IL-2 | - |
dc.title | Sodium meta-arsenite prevents the development of autoimmune diabetes in NOD mice | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000353864000016 | - |
dc.identifier.doi | 10.1016/j.taap.2014.12.016 | - |
dc.identifier.bibliographicCitation | TOXICOLOGY AND APPLIED PHARMACOLOGY, v.284, no.2, pp.254 - 261 | - |
dc.identifier.scopusid | 2-s2.0-84932131882 | - |
dc.citation.endPage | 261 | - |
dc.citation.startPage | 254 | - |
dc.citation.title | TOXICOLOGY AND APPLIED PHARMACOLOGY | - |
dc.citation.volume | 284 | - |
dc.citation.number | 2 | - |
dc.contributor.affiliatedAuthor | Lee, Y. S. | - |
dc.contributor.affiliatedAuthor | Kim, D. | - |
dc.contributor.affiliatedAuthor | Lee, E. K. | - |
dc.contributor.affiliatedAuthor | Choi, C. S. | - |
dc.contributor.affiliatedAuthor | Jun, H. S. | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Sodium meta-arsenite | - |
dc.subject.keywordAuthor | Type 1 diabetes | - |
dc.subject.keywordAuthor | Autoimmune | - |
dc.subject.keywordAuthor | Proliferation | - |
dc.subject.keywordAuthor | Glut1 | - |
dc.subject.keywordAuthor | Non-obese diabetic mice | - |
dc.subject.keywordPlus | ACTIVATED T-CELLS | - |
dc.subject.keywordPlus | CYTOKINE SECRETION | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | CANCER-CELLS | - |
dc.subject.keywordPlus | PROLIFERATION | - |
dc.subject.keywordPlus | LYMPHOCYTES | - |
dc.subject.keywordPlus | TRIOXIDE | - |
dc.subject.keywordPlus | INVOLVEMENT | - |
dc.subject.keywordPlus | DISEASE | - |
dc.subject.keywordPlus | IL-2 | - |
dc.relation.journalResearchArea | Pharmacology & Pharmacy | - |
dc.relation.journalResearchArea | Toxicology | - |
dc.relation.journalWebOfScienceCategory | Pharmacology & Pharmacy | - |
dc.relation.journalWebOfScienceCategory | Toxicology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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