7-O-galloyl-D-sedoheptulose is a novel therapeutic agent against oxidative stress and advanced glycation endproducts in the diabetic kidney.
Biol Pharm Bull
; 32(4): 657-64, 2009 Apr.
Article
en En
| MEDLINE
| ID: mdl-19336901
Diabetes is the leading cause of end-stage renal failure, since glucose-dependent metabolic factors are synergistically activated within the diabetic kidney. Accordingly, in Japan, there is much debate over the health benefits of natural therapies to reduce these risk factors. In our previous study, we reported that Cornus officinalis SIEB. et ZUCC. possessed an antidiabetic effect via ameliorating glucose-mediated metabolic disorders as well as aminoguanidine, an inhibitor of advanced glycation endproduct (AGE) formation, with a renoprotective effect. The aim of the present study was to investigate the effect of 7-O-galloyl-D-sedoheptulose (GS) against diabetic oxidative stress and AGE formation. Streptozotocin-induced diabetic rats were orally administered GS for 20 d, and the changes in serum glucose levels, as well as those of body weight every 10 d were evaluated. In addition, glucose, fluorescent AGE, methylglyoxal, glycolaldehyde (GA), and immunoblotting analyses for heme oxygenase-1, receptor for AGE, N(epsilon)-(carboxymethyl)lysine, N(epsilon)-(carboxyethyl)lysine, and GA-pyridine were performed in the kidney at the end of the experiment. The results obtained in this study demonstrated that 20 d of treatment with GS had beneficial effects on hypoglycemic and renal metabolic abnormalities, including renal glucose, oxidative stress, and AGE formation. Together, our data help to elucidate its potential therapeutic value against diabetic kidney disease.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Productos Finales de Glicación Avanzada
/
Estrés Oxidativo
/
Nefropatías Diabéticas
/
Heptosas
/
Antioxidantes
Tipo de estudio:
Risk_factors_studies
Límite:
Animals
Idioma:
En
Revista:
Biol Pharm Bull
Asunto de la revista:
BIOQUIMICA
/
FARMACOLOGIA
Año:
2009
Tipo del documento:
Article
País de afiliación:
Japón
Pais de publicación:
Japón