期刊
TOXICOLOGY AND APPLIED PHARMACOLOGY
卷 235, 期 1, 页码 57-67出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.taap.2008.11.007
关键词
Nrf2; Sulforaphane; NF-kappa B; beta cells; Cytokine
资金
- Ministry of Science and Technology (MOST)/Korea Science and Engineering Foundation (KOSEF) through the Diabetes Research Center at Chonbuk National University [R73-2008-005-0000-0]
- National Research Foundation of Korea [2008-0062328] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Sulforaphane (SFN) is an indirect antioxidant that protects animal tissues from chemical or biological insults by stimulating the expression of several NF-E2-related factor-2 (Nrf2)-regulated phase 2 enzymes. Treatment of RINm5F insulinoma cells with SFN increases Nrf2 nuclear translocation and expression of phase 2 enzymes. In this study, we investigated whether the activation of Nrf2 by SFN treatment or ectopic overexpression of Nrf2 inhibited cytokine-induced beta-cell damage. Treatment of RIN cells with IL-1 beta and IFN-gamma induced beta 3-cell damage through a NF-kappa B-dependent signaling pathway. Activation of Nrf2 by treatment with SFN and induction of Nrf2 overexpression by transfection with Nrf2 prevented cytokine toxicity. The mechanism by which Nrf2 activation inhibited NF-kappa B-dependent cell death signals appeared to involve the reduction of oxidative stress, as demonstrated by the inhibition of cytokine-induced H2O2 production. The protective effect of SFN was further demonstrated by the restoration of normal insulin secreting responses to glucose in cytokine-treated rat pancreatic islets. Furthermore, pretreatment with SFN blocked the development of type 1 diabetes in streptozotocin-treated mice. (C) 2008 Elsevier Inc. All rights reserved.
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