Affiliation:
1. University of Navarra, Department of Nutrition, Food Science and Physiology, Edificio de Investigación, C/Irunlarrea 1, Pamplona 31008, Spain
2. University of Navarra, Centre for Nutrition Research, Faculty of Pharmacy and Nutrition, Edificio de Investigación, C/Irunlarrea 1, Pamplona 31008, Spain
Abstract
In a recent issue of Clinical Science, Prieto-Vicente et al. [Clin. Sci. (2018) 132, 985–1001] have smartly demonstrated a potential new use of cardiotrophin-1 (CT-1) to treat and palliate an inflammatory bowel disease such as ulcerative colitis. In that work, authors report that in ulcerative colitic mice, administration of exogenous recombinant CT-1 (rCT-1) promotes lower colon damage and lower disease activity index, reducing systemic levels of tumor necrosis factor α (TNF-α) and also diminishing TNF-α expression in colon together with the reduction in other common inflammation markers. Besides, in vivo rCT-1 administration induces activation of several molecular pathways, including nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) and signal transducer and activator of transcription (STAT)-3, and abolishes bacterial translocation from intestine to other organs, including mesenteric ganglia, lungs, and spleen. Additionally, these results were nicely corroborated in CT-1 depleted mice; in which colon damage and ulcerative colitis severity were greater compared with the wild-type counterparts. All together, these results suggested that CT-1 could be a promising new therapeutic approach for treating inflammatory bowel disease, particularly ulcerative colitis. However, further studies are required to determine its major mechanisms of action and the potential efficacy of CT-1 in human inflammatory bowel diseases.
Cited by
2 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献