%0 Journal Article
%T Soybean and fish oil mixture increases IL-10, protects against DNA damage and decreases colonic inflammation in rats with dextran sulfate sodium (DSS) colitis
%A Karina V Barros
%A Roberta AN Xavier
%A Gilclay G Abreu
%A Carlos AR Martinez
%A Marcelo L Ribeiro
%A Alessandra Gambero
%A Patr¨ªcia O Carvalho
%A Claudia MO Nascimento
%A Vera LF Silveira
%J Lipids in Health and Disease
%D 2010
%I BioMed Central
%R 10.1186/1476-511x-9-68
%X Ulcerative colitis (UC) is an inflammatory bowel disease (IBD) characterized by recurrent episodes of colonic inflammation and tissue regeneration[1]. Although the pathogenesis of UC has not been entirely elucidated, the chronic relapsing inflammation has a multifactorial etiology. UC can be caused by an exaggerated immune response to the intestinal flora in the context of genetic predisposition [2,3] that can be attributed, at least in part, to an imbalance between effector T cells (Teff) and regulatory T cells (Treg)[4].In IBD, there is increased synthesis and release of pro-inflammatory mediators, such as eicosanoids, platelet activating factor, reactive oxygen species (ROS), nitrogen metabolites, chemokines and mainly cytokines [5] that have been associated with disease severity, activity and remission [2].Active episodes of UC are characterized by mucosal injury, increased vascular permeability, infiltration of neutrophilic polymorphonuclear, leukocytes, disruption of extracellular matrix and epithelial cell damage where the synthesis and release of ROS, triggered mainly by neutrophils, can mediate cell and tissues injury [6].Patients with IBD are at increased risk of developing colorectal cancer, and the inflammation has been associated with neoplastic changes through production of pro-inflammatory cytokines and ROS[7]. Both mediators activate nuclear transcription factor-kB (NF-kB), inducible nitric oxide synthesis, and cyclooxygenase-2-related signaling pathways, which may retard or suppress apoptosis in intestinal epithelial cells and modulate angiogenesis [8]. ROS, the cellular consequences of oxidative stress, may cause DNA oxidation, resulting in damage to all four bases and the deoxy-ribose-molecule [9,10]. Chronic inflammation in the colonic mucosa caused by increased and continuous exposure of ROS promotes oxidative DNA damage of the epithelial cells, triggering the appearance of genetic mutations and initiating colorectal carcinogenesis [10,11].Distu
%U http://www.lipidworld.com/content/9/1/68