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Título

Protection by nitric oxide against liver inflammatory injury in animals carrying a nitric oxide synthase-2 transgene

AutorMojena, Marina; Hortelano, Sonsoles; Castrillo, Antonio ; Díaz-Guerra, María José; García-Barchino, María J.; Sáez, Guillermo T.; Boscá, Lisardo
Palabras claveLiver cells
Lipopolysaccharide
Fecha de publicaciónmar-2001
EditorFederation of American Societies for Experimental Biology
CitaciónFaseb Journal 15(3): 583-585 (2001)
ResumenThe effect of pre-existent hepatic NO synthesis on liver injury induced by lipopolysaccharide was studied in animals carrying a nitric oxide synthase-2 (NOS-2) transgene under the control of the phosphoenolpyruvate carboxykinase (PEPCK) promoter. These animals expressed NOS-2 in liver cells under fasting conditions. Lipopolysaccharide-induced liver injury in D-galactosamine-conditioned mice, which enhanced notably the effect of the endotoxin on the liver, was impaired in animals expressing NOS-2. This protection against inflammatory liver damage was dependent on NO synthesis and was caused by an inhibition of nuclear factor kB (NF-kB) activity and an impairment of the synthesis of the proinflammatory cytokines tumor necrosis factor a and interleukin 1b. These data indicate that intrahepatic synthesis of NO protects liver by inhibiting the release of cascades of proinflammatory mediators and suggest a beneficial role for local delivery of NO in the control of liver injury.
Descripción22 pages, 7 figures, 1 table.
Versión del editorhttp://dx.doi.org/10.1096/fj.00-0509fje
URIhttp://hdl.handle.net/10261/24464
DOI10.1096/fj.00-0509fje
ISSN0892-6638
10.1096/fj.00-0509fje
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