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Muller, D.* ; Heissmeyer, V.* ; Dechend, R.* ; Hampich, F.* ; Park, J.* ; Fiebeler, A.* ; Shagdarsuren, E.* ; Theuer, J.* ; Elger, M.* ; Pilz, B.* ; Breu, V.* ; Schroer, K.* ; Ganten, D.* ; Dietz, R.* ; Haller, H.* ; Scheidereit, C.* ; Luft, F.*

Aspirin inhibits NF-kappa B and protects from angiotensin II-induced organ damage.

FASEB J. 15, 1822-+ (2001)
DOI Verlagsversion bestellen
Angiotensin (Ang)-II induces vascular wall inflammation by activating NF-kappaB. Aspirin inhibits IKK beta in vitro; however, the in vivo relevance of the phenomenon is unclear. We tested the hypothesis that aspirin protects from Ang II-induced endorgan damage by inhibiting NF-kappaB activation in vivo. Rats harboring human renin and angiotensinogen genes received high- (600 mg/kg/day) or low- (25 mg/kg/day) dose aspirin. High-dose aspirin reduced mortality, cardiac hypertrophy, fibrosis, and albuminuria independent of blood pressure, whereas both doses reduced cyclooxygenase activity. High-dose aspirin inhibited NF-kappaB and AP-1 activation and inflammation in heart and kidney. These in vivo results serve to explain the clinical utility of high- dose aspirin in inflammatory disorders and suggest additional therapeutic avenues that may be relevant to cardiovascular disease.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Angiotensin Ii ; Aspirin, Nf-kappa B ; End-organ Damage ; Inflammation; Nonsteroidal Antiinflammatory Drugs; Sodium-salicylate; Transcription Factor; Kinase-activity; Tissue Factor; Ikk Complex; Activation; Mechanisms; Cells; Renin
ISSN (print) / ISBN 0892-6638
e-ISSN 1530-6860
Zeitschrift FASEB Journal
Quellenangaben Band: 15, Heft: 8, Seiten: 1822-+ Artikelnummer: , Supplement: ,
Verlag Wiley
Verlagsort Bethesda, Md.
Begutachtungsstatus Peer reviewed