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Mol Med Rep ; 8(4): 1125-9, 2013 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-23942946

RESUMEN

The aim of this study was to determine the therapeutic efficacy of lactoferrin (Lf) on dextran sulphate sodium (DSS)­induced experimental colitis in BALB/c mice. Eighty BALB/c mice were randomly divided into 4 groups; the normal, model, apo­Lf and holo­Lf groups. Fecal character, fecal occult blood, hematochezia and disease activity index (DAI) were recorded daily. The length of the colon was measured and histological scores were evaluated 28 days post­treatment. Myeloperoxidase (MPO) activity was also determined and the expression of interleukin­1ß (IL­1ß) and tumor necrosis factor-α (TNF­α) were measured by quantitative (q)PCR. Lf relieved the inflammatory condition of DSS­induced experimental colitis in mice. The DAI and histological scores of Lf­treated mice were lower compared with those of mice in the control group. The length of the colon of Lf­treated mice was longer compared with that of mice in the control group. Treatment with Lf decreased MPO activity and the expression levels of IL­1ß and TNF­α. In addition, Lf was found to promote beneficial effects in a mouse model of experimental colitis. Treatment with apo­Lf was superior to that of holo­Lf in the mouse model of DSS­induced experimental colitis. Supplemental therapy with apo­Lf may provide an important new tool in the clinical management of ulcerative colitis.


Asunto(s)
Antiinflamatorios/farmacología , Colitis Ulcerosa/tratamiento farmacológico , Lactoferrina/farmacología , Animales , Antiinflamatorios/uso terapéutico , Colitis Ulcerosa/inducido químicamente , Colon/efectos de los fármacos , Colon/enzimología , Colon/patología , Sulfato de Dextran , Evaluación Preclínica de Medicamentos , Expresión Génica/efectos de los fármacos , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Lactoferrina/uso terapéutico , Masculino , Ratones , Ratones Endogámicos BALB C , Fragmentos de Péptidos/genética , Fragmentos de Péptidos/metabolismo , Peroxidasa/metabolismo
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