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Oxidative Medicine and Cellular Longevity
Volume 2013 (2013), Article ID 210563, 9 pages
http://dx.doi.org/10.1155/2013/210563
Research Article

Carbon Monoxide Attenuates Dextran Sulfate Sodium-Induced Colitis via Inhibition of GSK-3β Signaling

1School of Biological Sciences, University of Ulsan, Ulsan 680-749, Republic of Korea
2Department of Thoracic and Cardiovascular Surgery, Affiliated Hospital of Yanbian University, Yanji 133000, China
3Department of Anatomy, School of Medicine, Institute of Health Sciences, Gyeongsang National University, Jinju 660-701, Republic of Korea

Received 17 September 2013; Accepted 9 October 2013

Academic Editor: Alfredo Vannacci

Copyright © 2013 Md. Jamal Uddin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Endogenous carbon monoxide (CO) is produced by heme oxygenase-1 (HO)-1 which mediates the degradation of heme into CO, iron, and biliverdin. Also, CO ameliorates the human inflammatory bowel diseases and ulcerative colitis. However, the mechanism for the effect of CO on the inflammatory bowel disease has not yet been known. In this study, we showed that CO significantly increases survival percentage, body weight, colon length as well as histologic parameters in DSS-treated mice. In addition, CO inhalation significantly decreased DSS induced pro-inflammatory cytokines by inhibition of GSK-3β in mice model. To support the in vivo observation, TNF-α, iNOS and IL-10 after CO and LiCl treatment were measured in mesenteric lymph node cells (MLNs) and bone marrow-derived macrophages (BMMs) from DSS treated mice. In addition, we determined that CO potentially inhibited GSK-3β activation and decreased TNF-α and iNOS expression by inhibition of NF-κB activation in LPS-stimulated U937 and MLN cells pretreated with CO. Together, our findings indicate that CO attenuates DSS-induced colitis via inhibition of GSK-3β signaling in vitro and in vivo. Importantly, this is the first report that investigated the molecular mechanisms mediated the novel effects of CO via inhibition GSK-3β in DSS-induced colitis model.