Abstract Title:

Sulforaphane protects against cytokine- and streptozotocin-induced beta-cell damage by suppressing the NF-kappaB pathway.

Abstract Source:

Toxicol Appl Pharmacol. 2009 Feb 15;235(1):57-67. Epub 2008 Nov 21. PMID: 19071154

Abstract Author(s):

Mi-Young Song, Eun-Kyung Kim, Woo-Sung Moon, Jin-Woo Park, Hyung-Jin Kim, Hong-Seob So, Raekil Park, Kang-Beom Kwon, Byung-Hyun Park

Article Affiliation:

Department of Biochemistry, Medical School and Diabetes Research Center, Chonbuk National University, Jeonju, Jeonbuk, 561-756, Republic of Korea.


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-1beta and IFN-gamma induced beta-cell damage through a NF-kappaB-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-kappaB-dependent cell death signals appeared to involve the reduction of oxidative stress, as demonstrated by the inhibition of cytokine-induced H(2)O(2) 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.

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