Your browser doesn't support javascript.
loading
Montrer: 20 | 50 | 100
Résultats 1 - 1 de 1
Filtre
Ajouter des filtres








Gamme d'année
1.
Biol. Res ; 52: 50-50, 2019. ilus, graf
Article Dans Anglais | LILACS | ID: biblio-1505770

Résumé

BACKGROUND: Ureteral obstruction causes injury of the renal tissues and can irreversibly progress to renal fibrosis, with atrophy and apoptosis of tubular cells. The goal of the current study was to examine the effects of rhein on the apoptosis o renal tubular cells as well as renal fibrosis using a rodent model of unilateral ureteral obstruction (UUO). METHODS: UUO was induced through ureteral ligation, then animals received treatments with rhein or vehicle. The control rats only received sham operation. The renal tissue was harvested 1 week after surgery for assessment of kidney fibrosis. RESULTS: The expressions of collagen I and α-smooth muscle actin (α-SMA), as well as the severity of renal tubular apoptosis and fibrosis were time-dependently increased following UUO. Treatments with rhein partially inhibited such responses. Renal interstitial fibrosis was associated with STAT3 (signal transducer and activator of transcription 3) phosphorylation as well as altered expressions of Bax and Bcl2, both apoptosis-related proteins. Treatment with rhein also partly blocked these responses. CONCLUSION: These findings demonstrated that rhein mitigated apoptosis of renal tubular cell as well as renal fibrosis in a UUO rodent model. This curative effect is likely mediated via suppression of STAT3 phosphorylation.


Sujets)
Animaux , Mâle , Rats , Obstruction urétérale/prévention et contrôle , Anthraquinones/administration et posologie , Apoptose/effets des médicaments et des substances chimiques , Rein/anatomopathologie , Phosphorylation , Obstruction urétérale/métabolisme , Obstruction urétérale/anatomopathologie , Fibrose/métabolisme , Fibrose/anatomopathologie , Fibrose/prévention et contrôle , Rat Sprague-Dawley , Évolution de la maladie , Modèles animaux de maladie humaine , Facteur de transcription STAT-3/métabolisme
SÉLECTION CITATIONS
Détails de la recherche