Browsing by Subject "Colitis"

Now showing 1 - 4 of 4
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    Anti-inflammatory effects of enemas containing an oily extract of curcumin in an experimental model of diversion colitis
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Jaoudat Kadri, Caled; Aires Pereira, José; Guilherme Campos, Fábio; Marques Ortega, Manoela; Benediti Bragion, Celene; Real Martinez, Carlos Augusto
    Curcumin has powerful anti-inflammatory and antioxidant effects and it has been used for treatment of distal ulcerative colitis. The therapeutic effects of curcumin have not yet been evaluated in diversion colitis. The aim of the present study was to evaluate the anti-inflammatory effects of curcumin on colonic mucosa devoid of a faecal stream. Thirty-six rats were subjected to a proximal colostomy and distal colonic fistulation. They were divided into two groups, which were sacrificed two or four weeks after the intervention. Each group was divided into three subgroups treated with the daily application of enemas containing saline or an oily extract of curcumin at 50 mg/kg/day or 200 mg/kg/day. Colitis was diagnosed by histological analysis. Inflammatory grades were assessed using a previously validated scoring system. The infiltration of neutrophils was evaluated based on the tissue expression of myeloperoxidase (MPO), as determined by immunohistochemistry, and a computer-assisted image analysis program. The Mann-Whitney test was used to compare inflammation grades and myeloperoxidase levels among groups, and ANOVA was used to verify the variance over time, with the level of significance set at 5% (p<0.05) for both tests. Enemas containing curcumin improved the inflammation of the mucosa without a faecal stream and reduced the tissue contents of MPO. MPO tissue levels did not vary with time or between the concentrations of curcumin used. Enemas with curcumin improved the inflammation of the colonic mucosa, reduced the inflammatory grade and decreased the tissue content of MPO in colon segments without a faecal stream.
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    Caracterización de las bases genético-moleculares y ambientales relacionadas con la variabilidad interindividual en la respuesta a ANTI-TNF en pacientes con enfermedad inflamatoria intestinal.
    (2013-09-04) Lacruz Guzmán, Diana; Vicente Ortega, Vicente; Conesa Zamora, Pablo; Departamento de Oftalmología, Optometría, Otorrinolaringología y Anatomía Patológica
    Objetivo: investigar la relación entre la respuesta a los tratamientos anti-TNF en pacientes con EII y factores genéticos y ambientales. Método: estudio longitudinal de todos los pacientes con EII de un Hospital Universitario, en tratamiento con terapias anti-TNF. La respuesta al tratamiento se determinó mediante el uso del cuestionario CDAI (enfermedad de Crohn), y la determinación de las concentraciones séricas de proteína C reactiva. Los factores genéticos y bioquímicos se estudiaron mediante la identificación de polimorfismos tipo SNP y medición de concentraciones séricas de diversas citocinas. Resultados: Los pacientes con CU presentaron una mayor concentración sérica basal de citocinas (IL1, IL6, TNFα) que los pacientes con EC. Se observó asociación entre una mayor concentración sérica de IL1 y el genotipo CC del polimorfismo rs1143634 del gen de la IL1B. El alelo G del polimorfismo rs767455 del gen del TNFR1A mostró asociación con no respuesta clínica en pacientes con EC. Palabras clave: enfermedad inflamatoria intestinal, factores genéticos, respuesta, infliximab Objective: To investigate the relationship between the response to anti-TNF treatment in patients with IBD and genetic and environmental factors. Method: longitudinal study of all patients with IBD in a university hospital, treated with anti-TNF therapies. The response to treatment was determined by using the questionnaire CDAI (Crohn's disease), and determination of serum C-reactive protein. Biochemical and genetic factors were studied by identifying polymorphisms SNP type and measuring serum concentrations of various cytokines. Results: Patients with UC had a higher baseline serum cytokines (IL1, IL6, TNF) that patients with CD. Association was observed between increased serum IL1 and CC genotype rs1143634 polymorphism IL1B gene. The G allele of rs767455 polymorphism TNFR1A gene showed no association with clinical response in patients with CD. Key words: inflammatory bowel disease, genetic factors, response, infliximab.
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    NAD+ precursors and intestinal inflammation: therapeutic insights involving gut microbiota
    (MDPI, 2023-06-30) Niño-Narvión, Julia; Rojo-López, Marina Idalia; Martinez-Santos, Patricia; Rossell, Joana; Ruiz Alcaraz, Antonio José; Alonso, Núria; Ramos-Molina, Bruno; Mauricio, Didac; Julve, Josep; Bioquímica y Biología Molecular B e Inmunología; Facultad de Biología
    The oxidized form of nicotinamide adenine dinucleotide (NAD+) is a critical metabolite for living cells. NAD+ may act either as a cofactor for many cellular reactions as well as a coenzyme for different NAD+-consuming enzymes involved in the physiological homeostasis of different organs and systems. In mammals, NAD+ is synthesized from either tryptophan or other vitamin B3 intermediates that act as NAD+ precursors. Recent research suggests that NAD+ precursors play a crucial role in maintaining the integrity of the gut barrier. Indeed, its deficiency has been associated with enhanced gut inflammation and leakage, and dysbiosis. Conversely, NAD+-increasing therapies may confer protection against intestinal inflammation in experimental conditions and human patients, with accumulating evidence indicating that such favorable effects could be, at least in part, mediated by concomitant changes in the composition of intestinal microbiota. However, the mechanisms by which NAD+-based treatments affect the microbiota are still poorly understood. In this context, we have focused specifically on the impact of NAD+ deficiency on intestinal inflammation and dysbiosis in animal and human models. We have further explored the relationship between NAD+ and improved host intestinal metabolism and immunity and the composition of microbiota in vivo. Overall, this comprehensive review aims to provide a new perspective on the effect of NAD+-increasing strategies on host intestinal physiology.
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    Therapeutic effects of an azaphenothiazine derivative in mouse experimental colitis
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Artym, Jolanta; Kocięba, Maja; Zaczyńska, Ewa; Zimecki, Michał; Kałas, Wojciech; Strządała, Leon; Pawlak, Alicja; Jeleń, Małgorzata; Morak Młodawska, Beata; Pluta, Krystian; Kaleta Kuratewicz, Katarzyna; Madej, Jan P.; Kuropka, Piotr; Kuryszko, Jan
    Phenothiazines represent a class of compounds of potential therapeutic utility. In this report we evaluated therapeutic value of an azaphenothiazine derivative, 6-acetylaminobutyl-9-chloroquino[3,2- b]benzo[1,4]thiazine (QBT), given intragastrically, in the model of dextran sodium sulfate-induced colitis in C57BL/6 mice using 5-aminosalicylic acid (5-ASA) as a reference drug. Colitis symptoms such as body weight loss, diarrhea and hematochezia (blood in stool) were observed and registered and disease activity index (DAI) was calculated. In addition, weight and cell numbers in the lymphatic organs and histological parameters of the colon wall were analyzed. The effects of QBT on viability of colon epithelial cell lines were also determined. We showed that weight and cell number of draining mesenteric lymph nodes were lower in mice treated with QBT in comparison to their control counterparts. The number of thymocytes, drastically reduced in control mice, was elevated in mice treated with the compounds with a significant effect of 5-ASA. In addition, an abnormal composition of blood cell types was partially corrected in these groups. Histological analysis of the colon revealed that the pathological changes were partially normalized by QBT and even to a higher degree by 5-ASA. In conclusion we demonstrated a therapeutic efficacy of the compound in amelioration of local and systemic pathological changes associated with chemically-induced colitis in mice. A possible mechanism of action of the compound is discussed.