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Titolo:
Pharmacologic modulators of nitric oxide exacerbate tubulointerstitial inflammation in proteinuric rats
Autore:
Rangan, GK; Wang, YP; Harris, DCH;
Indirizzi:
Fremantle Hosp, Renal Unit, Fremantle, WA 6959, Australia Fremantle Hosp Fremantle WA Australia 6959 Fremantle, WA 6959, Australia Univ Western Australia, Dept Pharmacol, Perth, WA 6009, Australia Univ Western Australia Perth WA Australia 6009 Perth, WA 6009, Australia Univ Sydney, Westmead Hosp, Dept Renal Med, Sydney, NSW 2006, Australia Univ Sydney Sydney NSW Australia 2006 al Med, Sydney, NSW 2006, Australia
Titolo Testata:
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
fascicolo: 8, volume: 12, anno: 2001,
pagine: 1696 - 1705
SICI:
1046-6673(200108)12:8<1696:PMONOE>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
NF-KAPPA-B; CHRONIC-RENAL-FAILURE; L-ARGININE; ADHESION MOLECULE-1; EXPRESSION; SYNTHASE; CELLS; KIDNEY; MACROPHAGES; INHIBITION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Rangan, GK Fremantle Hosp, Renal Unit, F Block,POB 480,Alma St, Fremantle,WA 6959, Australia Fremantle Hosp F Block,POB 480,Alma St Fremantle WA Australia 6959
Citazione:
G.K. Rangan et al., "Pharmacologic modulators of nitric oxide exacerbate tubulointerstitial inflammation in proteinuric rats", J AM S NEPH, 12(8), 2001, pp. 1696-1705

Abstract

Nitric oxide (NO) regulates inflammatory responses partly by cell-specificinhibition of the transcription factor nuclear factor kappaB (NF-kappaB). This study investigated the effect of continuous oral administration of an NO donor (molsidomine [Mol]), NO precursor (L-arginine [L-arg]), or selective inhibitors of inducible NO synthase (iNOS; aminoguanidine [AGI, L-N-6-(1-iminoethyl)lysine [L-NIL]) on the progression of tubulointerstitial inflammation and NF-kappaB activation in a nonimmune model of chronic glomerular disease (Adriamycin nephropathy [AN]), from day 8 until day 30 after disease induction. On day 30, rats with AN had heavy proteinuria, reduced creatinine clearance, and tubulointerstitial disease. Treatment with both AG and L-NIL exacerbated the progression of AN as evidenced by (1) increased renal cortical malondialdehyde; (2) reduced creatinine clearance; and (3) increased tubular atrophy, interstitial volume, and monocyte infiltration. Unexpectedly, Mol also increased renal malondialdehyde and worsened tubular injury, whereas L-arg had no effect. The increase in renal cortical NF-kappaB activation in AN was not altered by AG, L-NIL, or Mel, but the mRNA expressionof monocyte chemoattractant protein-1, interleukin-10, and osteopontin were elevated in these groups. Nitrite release from kidney slices reduced in AN. Treatment with Mol restored renal nitrite release to normal, whereas neither L-arg nor the NOS inhibitors had an effect. It is concluded that endogenous iNOS-derived NO has a protective role against tubulointerstitial injury and cytokine production in AN. However, the pro-oxidant activity of NO donors may limit their potential benefit in proteinuric renal disease.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/07/20 alle ore 14:57:33