Norwegian
Albanian
Arabic
Armenian
Azerbaijani
Belarusian
Bengali
Bosnian
Catalan
Czech
Danish
Deutsch
Dutch
English
Estonian
Finnish
Français
Greek
Haitian Creole
Hebrew
Hindi
Hungarian
Icelandic
Indonesian
Irish
Italian
Japanese
Korean
Latvian
Lithuanian
Macedonian
Mongolian
Norwegian
Persian
Polish
Portuguese
Romanian
Russian
Serbian
Slovak
Slovenian
Spanish
Swahili
Swedish
Turkish
Ukrainian
Vietnamese
Български
中文(简体)
中文(繁體)
British Journal of Pharmacology 1999-May

Tranilast inhibits protein kinase C-dependent signalling pathway linked to angiogenic activities and gene expression of retinal microcapillary endothelial cells.

Bare registrerte brukere kan oversette artikler
Logg inn Registrer deg
Koblingen er lagret på utklippstavlen
S Koyama
H Takagi
A Otani
K Suzuma
K Nishimura
Y Honda

Nøkkelord

Abstrakt

1. Tranilast, first developed as an anti-allergic drug, has been reported to inhibit vascular endothelial growth factor (VEGF)-induced angiogenesis and vasopermeability. To further clarify the inhibitory mechanism, we investigated the effects of tranilast on VEGF binding and subsequent intracellular signalling pathway linked to angiogenic activities and gene expression of bovine retinal microcapillary endothelial cells. 2. Tranilast significantly (P<0.01) inhibited VEGF, basic fibroblast growth factor (bFGF), and hypoxia conditioned media-induced BREC proliferation in a dose dependent manner with IC50's of 22, 82 and 10 microM, respectively. 3. VEGF-induced migration was also inhibited by tranilast in a dose dependent manner, with IC50 of 18 microM, and complete inhibition was observed at 300 microM (P<0.01). Tranilast suppressed VEGF-induced tube formation in a dose dependent manner with maximum (46%) inhibition observed at 300 microM (P<0.05). 4. Tranilast inhibited phorbol myristate acetate (PMA)-dependent stimulation of [3H]-thymidine incorporation and VEGF- and PMA-induced gene expression of integrin alpha v and c-fos in BREC. 5. Tranilast suppressed VEGF- and PMA-stimulated PKC activity in BREC. 6. Tranilast did not affect VEGF binding or VEGF-induced phosphorylation of tyrosine residues of VEGF receptor- and phospholipase Cgamma and their associated proteins. 7. These data suggest that tranilast might prove an effective inhibitor to prevent retinal neovascularization in ischaemic retinal diseases, and that its inhibitory effect might be through suppression of PKC-dependent signal transduction in BREC.

Bli med på
facebooksiden vår

Den mest komplette databasen med medisinske urter støttet av vitenskap

  • Fungerer på 55 språk
  • Urtekurer støttet av vitenskap
  • Urtegjenkjenning etter bilde
  • Interaktivt GPS-kart - merk urter på stedet (kommer snart)
  • Les vitenskapelige publikasjoner relatert til søket ditt
  • Søk medisinske urter etter deres effekter
  • Organiser dine interesser og hold deg oppdatert med nyheter, kliniske studier og patenter

Skriv inn et symptom eller en sykdom og les om urter som kan hjelpe, skriv en urt og se sykdommer og symptomer den brukes mot.
* All informasjon er basert på publisert vitenskapelig forskning

Google Play badgeApp Store badge