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Biochem Cell Biol ; 84(2): 157-66, 2006 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-16609696

RESUMEN

Shiga toxin (Stx) produced by enterohemorrhagic Escherichia coli is a critical factor in the onset of hemolytic uremic syndrome. The current study was designed to assess whether n-3 and (or) n-6 polyunsaturated fatty acids (PUFA) act as a valuable adjunct to prevent the cell injury of renal tubule cells in the emergence of HUS. The target cells, ACHN cells derived from human tubule epithelium, were cultured with each PUFA, then exposed to Stx-1 or Stx-2. The rank order of potency of PUFA to inhibit the cell death caused by each toxin was as follows: EPA > AA = DHA >> LNA. There were dose-response relations in the efficacy of each PUFA. No prophylactic effect was found in the cultures with LA. Immunofluorescence assays revealed that both the expression of the toxin receptor on ACHN cells and binding between the toxin and cells were unaffected by the PUFA. These results suggest that EPA is the most efficacious PUFA against the renal tubule cell injury caused by Stx, which may be assigned to an alteration in the intracellular pathway leading to cell death.


Asunto(s)
Ácidos Grasos Insaturados/farmacología , Túbulos Renales/efectos de los fármacos , Toxina Shiga/antagonistas & inhibidores , Toxina Shiga/toxicidad , Línea Celular , Supervivencia Celular/efectos de los fármacos , Relación Dosis-Respuesta a Droga , Células Epiteliales/efectos de los fármacos , Células Epiteliales/metabolismo , Células Epiteliales/patología , Escherichia coli/patogenicidad , Ácidos Grasos Omega-3/farmacología , Ácidos Grasos Omega-6/farmacología , Ácidos Grasos Insaturados/administración & dosificación , Síndrome Hemolítico-Urémico/etiología , Síndrome Hemolítico-Urémico/prevención & control , Humanos , Túbulos Renales/metabolismo , Túbulos Renales/patología , Receptores de Superficie Celular/metabolismo , Toxina Shiga/metabolismo , Toxina Shiga I/toxicidad , Toxina Shiga II/toxicidad , Trihexosilceramidas/metabolismo
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