Angiopoietins in Diabetic Nephropathy / 대한신장학회지
Korean Journal of Nephrology
;
: 311-319, 2007.
Artigo
em Coreano
| WPRIM
| ID: wpr-162650
ABSTRACT
PURPOSE:
It has been reported that angiopoietins and Tie-2 receptor play an important role in the maintenance of glomerular filtration barrier in various glomerulonephritis models. We studied the role of angiopoietins on renal injury in diabetes.METHODS:
In this study, we examined the changes of angiopoietin-1, angiopoietin-2, Tie-2 receptor, and nephrin expression in the experimental diabetic nephropathy and also determined whether these changes were modified by renoprotective intervention by angiotensin II receptor blocker, alpha-lipoic acid, and peroxisome proliferator activated receptor (PPAR)-agonist.RESULTS:
A marked increase in urinary albumin excretion and glomerular volume was observed in diabetic rats. Renal angiopoietin-2 and Tie-2 receptor expression were significantly higher in diabetic rats than in the control groups, with a significant reduction in renal angiopoietin-2 expression, albuminuria, and renal hypertrophy in angiotensin II receptor blocker-treated diabetic rats. And there was a significant reduction in renal Tie-2 expression and renal hypertrophy in alpha-lipoic acid-treated and PPAR-gamma agonist-treated diabetic rats.CONCLUSION:
These results demonstrate that the dysregulation of angiopoietins and Tie-2 receptor can lead to renal hypertrophy and albuminuria. Angiotensin II receptor blocker, alpha-lipoic acid, and PPAR-gamma agonist attenuated these changes in angiopoietins and/or Tie-2 expression and prevented the development of albuminuria and renal hypertrophy in vivo.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Receptores de Angiotensina
/
Ácido Tióctico
/
Peroxissomos
/
Receptor TIE-2
/
Angiopoietinas
/
Angiopoietina-1
/
Angiopoietina-2
/
Nefropatias Diabéticas
/
Albuminúria
/
Barreira de Filtração Glomerular
Limite:
Animais
Idioma:
Coreano
Revista:
Korean Journal of Nephrology
Ano de publicação:
2007
Tipo de documento:
Artigo
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