000095851 001__ 95851
000095851 005__ 20240122154814.0
000095851 0247_ $$2doi$$a10.1155/2014/982639
000095851 0248_ $$2sideral$$a87530
000095851 037__ $$aART-2014-87530
000095851 041__ $$aeng
000095851 100__ $$0(orcid)0000-0002-5797-3909$$aLatorre, Eva$$uUniversidad de Zaragoza
000095851 245__ $$aIL-10 counteracts proinflammatory mediator evoked oxidative stress in Caco-2 cells.
000095851 260__ $$c2014
000095851 5060_ $$aAccess copy available to the general public$$fUnrestricted
000095851 5203_ $$aOxidative stress is thought to play a key role in the development of intestinal damage in intestinal inflammatory diseases. Several molecules are involved in the intestinal inflammation, either as pro- or anti-inflammatory factors;however, their effects on intestinal oxidative stress seem to be controversial. This work analyzes the contribution of pro- and anti-inflammatory molecules to the balance of oxidative damage in intestinal epithelial cells, as well as their effects on cellular antioxidant enzyme activity. With this purpose, the lipid and protein oxidation, together with the activity of catalase, superoxide dismutase, and glutathione peroxidase, were determined in the Caco-2 cells treated with serotonin, adenosine, melatonin, and TNF??, as proinflammatory factors, and IL-10, as an anti-inflammatory cytokine.The results have shown that all the proinflammatory factors assayed increased oxidative damage. In addition, these factors also inhibited the activity of antioxidant enzymes in the cells, except melatonin. In contrast, IL-10 did not alter these parameters but was able to reduce the prooxidant effects yielded by serotonin, adenosine, melatonin, or TNF??, in part by restoring the antioxidant enzymes activities. In summary, proinflammatory factors may induce oxidative damage in intestinal epithelial cells, whereas IL-10 seems to be able to restore the altered redox equilibrium in Caco-2 cells.
000095851 536__ $$9info:eu-repo/grantAgreement/ES/DGA/ARAINF-012-2008$$9info:eu-repo/grantAgreement/ES/DGA/B022-13$$9info:eu-repo/grantAgreement/ES/DGA/B105-11$$9info:eu-repo/grantAgreement/ES/DGA-FSE/B61$$9info:eu-repo/grantAgreement/ES/MICINN-FEDER/BFU2010-18971
000095851 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000095851 590__ $$a3.236$$b2014
000095851 591__ $$aIMMUNOLOGY$$b58 / 147 = 0.395$$c2014$$dQ2$$eT2
000095851 591__ $$aCELL BIOLOGY$$b97 / 184 = 0.527$$c2014$$dQ3$$eT2
000095851 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000095851 700__ $$0(orcid)0000-0002-1605-0542$$aMatheus, Nyurky
000095851 700__ $$0(orcid)0000-0001-5573-6144$$aLayunta, Elena
000095851 700__ $$0(orcid)0000-0002-9935-927X$$aAlcalde, Ana Isabel$$uUniversidad de Zaragoza
000095851 700__ $$0(orcid)0000-0003-4758-3998$$aMesonero, José Emilio$$uUniversidad de Zaragoza
000095851 7102_ $$11005$$2410$$aUniversidad de Zaragoza$$bDpto. Farmacología y Fisiolog.$$cÁrea Fisiología
000095851 773__ $$g2014, 14 (2014), 982639 [6 pp]$$pMediat. inflamm.$$tMEDIATORS OF INFLAMMATION$$x0962-9351
000095851 8564_ $$s262730$$uhttps://zaguan.unizar.es/record/95851/files/texto_completo.pdf$$yVersión publicada
000095851 8564_ $$s32796$$uhttps://zaguan.unizar.es/record/95851/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000095851 909CO $$ooai:zaguan.unizar.es:95851$$particulos$$pdriver
000095851 951__ $$a2024-01-22-15:35:00
000095851 980__ $$aARTICLE