Role of p38 mitogen-activated protein kinase in the pathogenesis of stress ulcer / 中华外科杂志
Chinese Journal of Surgery
;
(12): 1284-1287, 2005.
Artículo
en Chino
| WPRIM
| ID: wpr-306120
ABSTRACT
<p><b>OBJECTIVE</b>To determine whether the activation of p38 mitogen-activated protein kinase (MAPK) is involved in the pathogenesis of stress ulcer.</p><p><b>METHODS</b>Model of stress ulcer was established with the treatment of rats with water-immersion restraint (WIR) stress. Ulcer index (UI) was macroscopically evaluated as a parameter of gastric mucosal lesions. Expression of phospho- and pan-p38 in gastric mucosa was detected using Western blot analysis. Tumor necrosis factor-alpha (TNF-alpha) and Interleukin 1beta (IL-1beta) gene expressions were analyzed by Northern blot analysis. As indicated in some experiments, rats were pretreated with intravenous injection of the specific p38 MAPK inhibitor CNI-1493 prior to WIR stress and then the changes of UI and TNF-alpha and IL-1beta mRNA expression were examined.</p><p><b>RESULTS</b>The p38 MAPK was persistently activated in the gastric mucosa of rats with WIR stress, with maximal activation after 1 h of stress [(6.8 +/- 3.2) fold of baseline levels, P < 0.01]. Inhibition of p38 MAPK activation with CNI-1493 led to a marked decrease in UI in WIR stress rats. Similarly, the increased gene expression of proinflammatory cytokines TNF-alpha and IL-1beta in gastric mucosa induced by WIR stress were significantly diminished by p38 MAPK inhibition.</p><p><b>CONCLUSION</b>p38 MAPK might have an important role in the pathogenesis of stress ulcer.</p>
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Fisiología
/
Úlcera Gástrica
/
Estrés Fisiológico
/
Interleucina-1
/
Factor de Necrosis Tumoral alfa
/
Ratas Sprague-Dawley
/
Proteínas Quinasas p38 Activadas por Mitógenos
/
Modelos Animales de Enfermedad
/
Genética
/
Metabolismo
Tipo de estudio:
Estudio de etiología
/
Estudio pronóstico
Límite:
Animales
Idioma:
Chino
Revista:
Chinese Journal of Surgery
Año:
2005
Tipo del documento:
Artículo
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