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pubmed-article:20081544pubmed:abstractTextInflammatory bowel disease (IBD) is characterized by recurrent and severe gastrointestinal inflammation. Activation of inflammatory cells, such as TH17 lymphocytes, and/or deficiency of regulatory T cells (Treg) are responsible for the pathogenesis of IBD. As an acute phase reactant, heme oxygenase-1 (HO-1) has been shown to play an anti-inflammatory and immunomodulatory role in many disease processes. In this study, we used a dextran sulfate sodium (DSS)-induced murine colitis model to investigate the effect of upregulating HO-1 by hemin on the development of colonic inflammation.lld:pubmed
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pubmed-article:20081544pubmed:articleTitleHemin exerts multiple protective mechanisms and attenuates dextran sulfate sodium-induced colitis.lld:pubmed
pubmed-article:20081544pubmed:affiliationDepartment of Pediatrics, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.lld:pubmed
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