Methionine restriction on oxidative stress and immune response in dss-induced colitis mice
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Gang Liu1, Lei Yu2, Jun Fang3, Chien-An Andy Hu1,4, Jie Yin1, Hengjia Ni1, Wenkai Ren1, Veeramuthu Duraipandiyan5, Shuai Chen1, Naif Abdullah Al-Dhabi5 and Yulong Yin1,6,7
1Key Laboratory of Agro-Ecological Processes in Subtropical Region, Institute of Subtropical Agriculture, Chinese Academy of Sciences, Changsha 410125, China
2China Animal Disease Control Center, Beijing 102618, China
3College of Bioscience and Biotechnology, Hunan Agricultural University, Changsha 410128, China
4Department of Biochemistry and Molecular Biology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131, USA
5Addiriyah Research Chair for Environmental Studies, Department of Botany and Microbiology, College of Science, King Saud University, Riyadh 11451, Saudi Arabia
6College of Animal Science, South China Agricultural University, Guangzhou 510642, China
7Laboratory of Animal Nutrition and Human Health, School of Life Sciences, Hunan Normal University, Changsha 410081, China
Wenkai Ren, email: [email protected]
Yulong Yin, email: [email protected]
Keywords: inflammatory bowel disease, methionine restriction, diet, oxidative stress, NF-κB
Received: December 28, 2016 Accepted: April 14, 2017 Published: May 11, 2017
A strong correlation exists between inflammatory bowel disease (IBD) and oxidative stress involving alterations of several key signaling pathways. It is known that methionine promotes reactive oxygen species (ROS) production; we therefore hypothesize that a methionine restriction diet would reduce ROS production, inflammatory responses, and the course of IBD. We generated a murine colitis model by dextran sodium sulfate (DSS) treatment and tested the effects of the methionine restriction diet. Forty-eight mice were randomly divided into four groups of equal size, which included a control (CON) group, an MR (methionine restriction diet) group, a DSS treated group and an MR-DSS treated group. Mice in the first two groups had unrestricted access to water for one week. Mice in the two DSS-treated groups had unrestricted access to 5% DSS solution supplied in the drinking water for the same period. Mice in the CON and DSS groups were given a basal diet, whereas mice in the MR-DSS and MR groups were fed a 0.14% MR diet. We found that DSS reduced daily weight gain, suppressed antioxidant enzyme expression, increased histopathology scores and activated NF-κB and nuclear factor erythroid 2-related factor 2/Kelch-like ECH-associated protein 1 (Nrf2/Keap1) signaling. We also showed that the MR diet upregulated catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities, decreased myeloperoxidase (MPO), TNF-α and IL-1β, and reversed activation of the NF-κB signaling pathway in MR-DSS mice. Taken together, our results imply that the MR diet may be considered as an adjuvant in IBD therapeutics.
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