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1.
Yonsei med. j ; Yonsei med. j;: 308-316, 2007.
Article de Anglais | WPRIM | ID: wpr-180514

RÉSUMÉ

PURPOSE: We recently reported that rosiglitazone (RGTZ), a peroxisome proliferator-activated receptor gamma (PPARgamma) agonist, has a protective effect against cyclosporine (CsA)- induced renal injury. Here we report the effect of RGTZ on peroxisome proliferator-activated receptor gamma (PPARgamma) expression in an experimental model of chronic cyclosporine (CsA) nephropathy. MATERIALS AND METHODS: Chronic CsA nephropathy was induced in Sprague-Dawley rats by administering CsA (15mg/kg per day) for 28 days, and control rats were treated with vehicle (VH group, olive oil 1mL/kg per day) for 28 days. RGTZ (3mg/kg) was concurrently administered via gavage to the CsA and VH groups. Expression of PPARgamma mRNA and protein was evaluated with RT-PCR, immunohistochemistry, and immunoblotting. RESULTS: PPARgamma mRNA expression was similar to the level of PPARgamma protein constitutively expressed in the kidneys of the VH treated rats, with expression in the glomerular epithelial, distal tubular cells, and collecting tubular cells. PPARgamma protein expression in CsA-treated rat kidneys was significantly less than in the VH group. However, concomitant administration of RGTZ restored PPARgamma protein expression in the kidneys of the CsA- reated rats. CONCLUSION: Exogenous administration of RGTZ treatment upregulates PPARgamma expression and that this mechanism may play a role in protecting against CsA-induced renal injury.


Sujet(s)
Rats , Mâle , Animaux , Transcription génétique/effets des médicaments et des substances chimiques , Thiazolidinediones/pharmacologie , Rat Sprague-Dawley , ARN messager/génétique , Biosynthèse des protéines/effets des médicaments et des substances chimiques , Récepteur PPAR gamma/génétique , Maladies du rein/génétique , Régulation de l'expression des gènes/effets des médicaments et des substances chimiques , Modèles animaux de maladie humaine , Ciclosporine/toxicité
2.
Yonsei med. j ; Yonsei med. j;: 517-525, 2007.
Article de Anglais | WPRIM | ID: wpr-71486

RÉSUMÉ

PURPOSE: Local activation of the complement system plays a role in target organ damage. The aim of our study was to investigate the influence of cyclosporine (CsA)- induced renal injury on the complement system in the kidney. MATERIALS AND METHODS: Mice fed a low salt (0.01%) diet were treated with vehicle (VH, olive oil, 1mL/kg/day) or CsA (30mg/kg/day) for one or four weeks. Induction of chronic CsA nephrotoxicity was evaluated with renal function and histomorphology. Activation of the complement system was assessed through analysis of the expression of C3, C4d, and membrane attack complex (MAC), and the regulatory proteins, CD46 and CD55. CsA treatment induced renal dysfunction and typical morphology (tubulointerstitial inflammation and fibrosis) at four weeks. RESULTS: CsA-induced renal injury was associated with increased the expression of C3, C4d, and MAC (C9 and upregulation of complement regulatory proteins (CD 46 and CD55). Immunohistochemistry revealed that the activated complement components were mainly confined to the injured tubulointerstitium. CONCLUSION: CsA-induced renal injury is associated with activation of the intrarenal complement system.


Sujet(s)
Animaux , Souris , Antigènes CD45/analyse , Antigènes CD46/analyse , Antigènes CD55/analyse , Complément C3/analyse , Complément C4b/analyse , Complexe d'attaque membranaire du complément/analyse , Protéines du système du complément/analyse , Ciclosporine/toxicité , Modèles animaux de maladie humaine , Immunité innée/effets des médicaments et des substances chimiques , Immunotransfert , Immunohistochimie , Immunosuppresseurs/toxicité , Rein/effets des médicaments et des substances chimiques , Maladies du rein/induit chimiquement , Microscopie confocale , Fragments peptidiques/analyse
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