期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 47, 期 12, 页码 1731-1741出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2009.09.020
关键词
Oxysterols; Colonic mucosa; NADPH oxidase; Reactive oxygen species; Apoptosis; Inflammatory bowel disease; Free radicals
资金
- European Science Foundation
- Italian Ministry of University
- PRIN 2006
- PRIN 2007
- Region of Piedmont (Ricerca Sanitaria Finalizzata) [200, 2007, 2008a, 2008b, 2009]
- University of Turin, Italy
With the aim of investigating whether cholesterol oxidation products could contribute to the pathogenesis of the intestinal epithelial barrier dysfunction that occurs in human inflammatory bowel disease (IBD), differentiated versus undifferentiated CaCo-2 cells, an accepted model for human intestinal epithelial cells, were challenged with a dietary-representative mixture of oxysterols. Only differentiated colonic cells were susceptible to the proapoptotic action of the oxysterol mixture, checked both by enzymatic and by morphological methods, mainly because of a very low AI(T phosphorylation pathway compared to the undifferentiated counterparts. Enhanced production of reactive oxygen species by a colonic NADPH oxidase hyperactivation seemed to represent the key event in oxysterol-induced up-regulation of the mitochondrial pathway of programmed death of differentiated CaCo-2 cells. These in vitro findings point to the pro-oxidant and cytotoxic potential of cholesterol oxidation products, of both dietary and endogenous origin, as an important mechanism of induction and/or worsening of the functional impairment of enteric mucosa that characterizes IBD. (C) 2009 Elsevier Inc. All rights reserved.
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