Logo del repository
  1. Home
 
Opzioni

SOD AND GSH INHIBIT THE HIGH GLUCOSE-INDUCED OXIDATIVE DAMAGE AND THE PDGF INCREASED SECRETION IN CULTURED HUMAN ENDOTHELIAL-CELLS

CURCIO, Francesco
•
PERRELLA, Giuseppina
•
CERIELLO, Antonio
altro
FALLETI E
1995
  • journal article

Periodico
THROMBOSIS AND HAEMOSTASIS
Abstract
Poor control of blood glucose has been established as a key pathogenetic mechanism in the vascular complications of diabetes. It has been reported that glucose may autooxidize generating free radicals which have been suggested to delay proliferation, to modify mobility, to influence platelet-derived growth factor and other secretory protein production in a variety of cell systems. Platelet-derived growth factor, in turn, may induce proliferation and migration of vascular smooth muscle cells and thus play a role in atherogenesis. In the present study the effects of antioxidants on the high glucose-dependent oxidative cell damage and increased platelet-derived growth factor secretion have been investigated using cultured human endothelial cells. Our findings show that rising the glucose concentration in the culture medium from 5 mM to 20 mM, increased the production of free radicals cell damage markers, such as malondialdehyde and conjugated dienes, as well as the production of platelet-derived growth factor. The addition of super oxide dismutase or glutathione prevents both such effects. These results suggest that antioxidants may be a helpful therapeutic adjuvant to reduce the vascular complications of diabetes.
WOS
WOS:A1995RV50400029
Archivio
http://hdl.handle.net/11390/880019
info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-0029084142
Diritti
metadata only access
Visualizzazioni
2
Data di acquisizione
Apr 19, 2024
Vedi dettagli
google-scholar
Get Involved!
  • Source Code
  • Documentation
  • Slack Channel
Make it your own

DSpace-CRIS can be extensively configured to meet your needs. Decide which information need to be collected and available with fine-grained security. Start updating the theme to match your nstitution's web identity.

Need professional help?

The original creators of DSpace-CRIS at 4Science can take your project to the next level, get in touch!

Realizzato con Software DSpace-CRIS - Estensione mantenuta e ottimizzata da 4Science

  • Impostazioni dei cookie
  • Informativa sulla privacy
  • Accordo con l'utente finale
  • Invia il tuo Feedback