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Clin Exp Immunol ; 167(2): 269-74, 2012 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-22236003

RESUMEN

The activation of nuclear factor-kappa B (NF-κB) in vascular endothelial cells may be involved in vascular pathogeneses such as vasculitis or atherosclerosis. Recently, it has been reported that some amino acids exhibit anti-inflammatory effects. We investigated the inhibitory effects of a panel of amino acids on cytokine production or expression of adhesion molecules that are involved in inflammatory diseases in various cell types. The activation of NF-κB was determined in human coronary arterial endothelial cells (HCAECs) because NF-κB modulates the production of many cytokines and the expression of adhesion molecules. We examined the inhibitory effects of the amino acids cysteine, histidine and glycine on the induction of NF-κB activation, expression of CD62E (E-selectin) and the production of interleukin (IL)-6 in HCAECs stimulated with tumour necrosis factor (TNF)-α. Cysteine, histidine and glycine significantly reduced NF-κB activation and inhibitor κBα (IκBα) degradation in HCAECs stimulated with TNF-α. Additionally, all the amino acids inhibited the expression of E-selectin and the production of IL-6 in HCAECs, and the effects of cysteine were the most significant. Our results show that glycine, histidine and cysteine can inhibit NF-κB activation, IκBα degradation, CD62E expression and IL-6 production in HCAECs, suggesting that these amino acids may exhibit anti-inflammatory effects during endothelial inflammation.


Asunto(s)
Antiinflamatorios/farmacología , Arteritis/prevención & control , Vasos Coronarios/citología , Cisteína/farmacología , Células Endoteliales/efectos de los fármacos , Glicina/farmacología , Histidina/farmacología , Células Cultivadas/efectos de los fármacos , Células Cultivadas/metabolismo , Evaluación Preclínica de Medicamentos , Selectina E/biosíntesis , Selectina E/genética , Células Endoteliales/metabolismo , Endotelio Vascular/citología , Regulación de la Expresión Génica/efectos de los fármacos , Humanos , Proteínas I-kappa B/metabolismo , Interleucina-6/biosíntesis , Interleucina-6/genética , Inhibidor NF-kappaB alfa , FN-kappa B/metabolismo , Factor de Necrosis Tumoral alfa/farmacología
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