ABSTRACT
TITLE: Utilidad de la resonancia magnetica craneal para el diagnostico de la distrofia miotonica de tipo 1.
Subject(s)
Magnetic Resonance Imaging , Myotonic Dystrophy/diagnostic imaging , Neuroimaging , White Matter/diagnostic imaging , Adult , Cerebral Cortex/diagnostic imaging , Cerebral Cortex/pathology , Corpus Callosum/diagnostic imaging , Corpus Callosum/pathology , Diffusion Magnetic Resonance Imaging , Humans , Magnetic Resonance Imaging/methods , Male , Myotonic Dystrophy/pathology , White Matter/pathologyABSTRACT
Extra virgin olive oil (EVOO) has demonstrated immunomodulatory and antiinflammatory properties in murine experimental ulcerative colitis (UC). In addition to its high monounsaturated fatty acid content, evidences have accumulated on the favorable properties of minor, although highly bioactive, components present in the unsaponifiable fraction (UF). The present study was designed to evaluate the effects of dietary EVOO's UF supplementation on acute UC. C57BL/6 mice were fed from weaning with sunflower oil (SD), EVOO diet and UF-enriched SD at 5% oil (SD+UF). After 30 days, mice were exposed to 3% dextran sulfate sodium (DSS) for 5 days developing acute colitis. After 4 days of DSS removal, animals were sacrificed and colons were histological and biochemically processed. Disease activity index and microscopic damage score were significantly improved in EVOO and SD+UF dietary groups versus SD group. In addition, both dietary treatments significantly induced decreases in MCP-1 and TNF-α levels, iNOS and COX-2 overexpression and p38 MAPKs activation in colon mucosa. Moreover, an upregulation of IκB expression was also observed after feeding the animals with both diets. However, no statistically differences between data from mice fed with EVOO or UF+SD diets were observed. Dietary enrichment with EVOO's UF reduces the damage in acute colitis model, alleviating the oxidative events and returning proinflammatory proteins expression to basal levels probably through p38 MAPK and NFκB signalling pathways. EVOO's UF diet might provide a basis for developing a new strategy in dietary supplementation for the prevention of UC.
Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Colitis, Ulcerative/prevention & control , Colon/immunology , Dietary Supplements , Intestinal Mucosa/immunology , Plant Extracts/therapeutic use , Plant Oils/chemistry , Animals , Chemokine CCL2/antagonists & inhibitors , Chemokine CCL2/genetics , Chemokine CCL2/metabolism , Colitis, Ulcerative/immunology , Colitis, Ulcerative/metabolism , Colitis, Ulcerative/pathology , Colon/metabolism , Colon/pathology , Cyclooxygenase 2/chemistry , Cyclooxygenase 2/genetics , Cyclooxygenase 2/metabolism , Enzyme Activation , Female , Gene Expression Regulation , Hydrolysis , Intestinal Mucosa/metabolism , Intestinal Mucosa/pathology , Mice, Inbred C57BL , Nitric Oxide Synthase Type II/antagonists & inhibitors , Nitric Oxide Synthase Type II/genetics , Nitric Oxide Synthase Type II/metabolism , Olive Oil , Plant Oils/standards , Random Allocation , Tumor Necrosis Factor-alpha/antagonists & inhibitors , Tumor Necrosis Factor-alpha/genetics , Tumor Necrosis Factor-alpha/metabolism , Weaning , p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors , p38 Mitogen-Activated Protein Kinases/metabolismABSTRACT
Current epidemiological and experimental studies support a beneficial role of dietary polyphenols in several gastrointestinal diseases, including inflammatory bowel disease. The aim of this study was to gain a better understanding of the effects of a naturally occurring polyphenol, ellagic acid, present in some fruits such as pomegranate, raspberries and nuts among others, in an experimental murine model of Crohn's disease by intra-colonic administration of TNBS in rats. Analysis of the lesions were carried out by macroscopic and histological technics. Inflammation response was assessed by histology and myeloperoxidase activity. iNOS and COX-2 are upregulated by MAPKs and NF-κB nuclear transcription factor in intestinal epithelial cells thus, we determined the expression of iNOS, COX-2 and the involvement of the p38, JNK, ERK1/2 MAPKs and NF-κB signalling in the protective effect of EA by western blotting. Oral administration of EA (10-20 mg/kg) diminished the severity and extension of the intestinal injuries induced by TNBS although there was no observed a significant dose-response. In addition, EA increased mucus production in goblet cells in colon mucosa, decreased neutrophil infiltration and pro-inflammatory proteins COX-2 and iNOS overexpression. Also EA was capable of reducing the activation of p38, JNK and ERK1/2 MAPKs, preventing the inhibitory protein IκB-degradation and inducing an inhibition of the nuclear translocation level of p65 in colonic mucosa. In conclusion, EA reduces the damage in a rat model of Crohn's disease, alleviates the oxidative events and returns pro-inflammatory proteins expression to basal levels probably through MAPKs and NF-κB signalling pathways.
