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Open AccessArticle

Dimethyl Fumarate Alleviates Dextran Sulfate Sodium-Induced Colitis, through the Activation of Nrf2-Mediated Antioxidant and Anti-inflammatory Pathways

1
Department of Surgery, University of California, Irvine, CA 92868, USA
2
Department of Pathology, University of California, Irvine, CA 92868, USA
3
Department of Medicine, University of California, Irvine, CA 92868, USA
*
Author to whom correspondence should be addressed.
Antioxidants 2020, 9(4), 354; https://doi.org/10.3390/antiox9040354
Received: 14 March 2020 / Revised: 21 April 2020 / Accepted: 22 April 2020 / Published: 24 April 2020
(This article belongs to the Special Issue Keap1/Nrf2 Signaling Pathway)
Oxidative stress and chronic inflammation play critical roles in the pathogenesis of ulcerative colitis (UC) and inflammatory bowel diseases (IBD). A previous study has demonstrated that dimethyl fumarate (DMF) protects mice from dextran sulfate sodium (DSS)-induced colitis via its potential antioxidant capacity, and by inhibiting the activation of the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome. This study aims to clarify the nuclear factor erythroid 2-related factor 2/antioxidant responsive element (Nrf2/ARE) pathway pharmacological activation and anti-inflammatory effect by DMF, through focusing on other crucial antioxidant enzymes and inflammatory mediator, including glutamate-cysteine ligase catalytic subunit (GCLC), glutathione peroxidase (GPX) and cyclooxygenase-2 (COX-2), in a DSS-induced colitis mouse model. The oral administration of DMF attenuated the shortening of colons and alleviated colonic inflammation. Furthermore, the expression of key antioxidant enzymes, including GCLC and GPX, in the colonic tissue were significantly increased by DMF administration. In addition, protein expression of the inflammatory mediator, COX-2, was reduced by DMF administration. Our results suggest that DMF alleviates DSS-induced colonic inflammatory damage, likely via up-regulating GCLC and GPX and down-regulating COX-2 protein expression in colonic tissue. View Full-Text
Keywords: colitis; Nrf2; dimethyl fumarate; antioxidant; anti-inflammation colitis; Nrf2; dimethyl fumarate; antioxidant; anti-inflammation
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MDPI and ACS Style

Li, S.; Takasu, C.; Lau, H.; Robles, L.; Vo, K.; Farzaneh, T.; Vaziri, N.D.; Stamos, M.J.; Ichii, H. Dimethyl Fumarate Alleviates Dextran Sulfate Sodium-Induced Colitis, through the Activation of Nrf2-Mediated Antioxidant and Anti-inflammatory Pathways. Antioxidants 2020, 9, 354. https://doi.org/10.3390/antiox9040354

AMA Style

Li S, Takasu C, Lau H, Robles L, Vo K, Farzaneh T, Vaziri ND, Stamos MJ, Ichii H. Dimethyl Fumarate Alleviates Dextran Sulfate Sodium-Induced Colitis, through the Activation of Nrf2-Mediated Antioxidant and Anti-inflammatory Pathways. Antioxidants. 2020; 9(4):354. https://doi.org/10.3390/antiox9040354

Chicago/Turabian Style

Li, Shiri; Takasu, Chie; Lau, Hien; Robles, Lourdes; Vo, Kelly; Farzaneh, Ted; Vaziri, Nosratola D.; Stamos, Michael J.; Ichii, Hirohito. 2020. "Dimethyl Fumarate Alleviates Dextran Sulfate Sodium-Induced Colitis, through the Activation of Nrf2-Mediated Antioxidant and Anti-inflammatory Pathways" Antioxidants 9, no. 4: 354. https://doi.org/10.3390/antiox9040354

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