Abstract
Oleoylethanolamide (OEA) is an endogenous fatty acid ethanolamide known for its anti-inflammatory effects and its influence on gut microbiota composition; however, the effects of OEA in inflammatory bowel disease (IBD) remain unknown. During in vitro experiments, OEA downregulated the expression of tumor necrosis factor (TNF)-α and reduced phosphorylation of inhibitor of kappa (Iκ) Bα induced by lipopolysaccharide in human embryonic kidney cells. Moreover, OEA downregulated the expression of interleukin (IL)-8 and IL-1β and inhibited the phosphorylation of IκBα and p65 induced by TNF-α in human enterocytes (Caco-2). The effect of OEA in reducing the expression of IL-8 was blocked by the peroxisome proliferator-activated receptor (PPAR)-α antagonist. During in vivo experiments on rats, colitis was induced by the oral administration of 8% dextran sulfate sodium from day 0 through day 5, and OEA (20 mg/kg) was intraperitoneally injected once a day from day 0 for 6 days. OEA administration significantly ameliorated the reduction in body weight, the increase in disease activity index score, and the shortening of colon length. In rectums, OEA administration reduced the infiltration of macrophages and neutrophils and tended to reduce the histological score and the expression of inflammatory cytokines. Administration of OEA produced significant improvement in a colitis model, possibly by inhibiting the nuclear factor kappa B signaling pathway through PPAR-α receptors. OEA could be a potential new treatment for IBD.
Highlights
Inflammatory bowel disease (IBD), which mainly consists of Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic inflammatory disorder of the gastrointestinal tract
Treatment with tumor necrosis factor (TNF)-a significantly upregulated the expression of interleukin (IL)-8 and IL-1b compared to control, and OEA significantly reduced the expression of IL-8 and IL-1b compared to TNF-a treatment (Figure 3A)
Western blotting demonstrated that treatment with TNF-a increased phosphorylation of IkBa and p65 compared to control, and OEA inhibited TNF-a-induced phosphorylation of IkBa and p65 in Caco-2 cells compared to TNF-a treatment (Figure 3B)
Summary
Inflammatory bowel disease (IBD), which mainly consists of Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic inflammatory disorder of the gastrointestinal tract. Due to the development of new therapeutic drugs for IBD in recent decades, such as biological medicines, treatment options have increased (Feagan et al, 2016; Sandborn et al, 2017); due to a lack of curative treatment for IBD, many patients remain resistant to medical therapy and require surgery (Peyrin-Biroulet et al, 2010; Fumery et al, 2018). New therapeutic options for IBD are needed. Previous studies have demonstrated that the administration of OEA has therapeutic effects on modulating feeding, lipid metabolism, and gastrointestinal motility (Cluny et al, 2009; Decara et al, 2012; Fu and Gaetani, 2013). Other studies have demonstrated that OEA has neuroprotective and antiatherosclerotic functions (Fan et al, 2014; Gonzalez-Aparicio et al, 2017). The effects and roles of OEA administration in IBD remain unknown
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
