Purchase this article with an account.
F. Lamoke, M. Labazi, D. Marcus, M. Bartoli; Trans-Chalcone Prevents VEGF Expression and Retinal Neovascularization in the Ischemic Retina. Invest. Ophthalmol. Vis. Sci. 2008;49(13):3984.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Retinal neovascularization (RNV) is an important pathological event and a major cause of blindness. Vascular inflammation and oxidative stress have been shown to play a role in the induction and progression of RNV. We characterized the effects of the flavonoid trans-chalcone in preventing RNV in a model of ischemic retinopathy. Trans-chalcone-derived flavonoids have been previously shown to be negative modulators of inflammatory responses as well as tumor angiogenesis.
Ischemic retinopathy was induced in neonatal mice following the protocol of the mouse model of oxygen-induced retinopathy (Smith, LEH. et al. 1994). Trans-chalcone was administered intra-peritoneum at the dose of 25mg/Kg/day. Vascular density was assessed by morphometric analysis of flat mounted retinas stained with Texas red-Isolectin B4. Western blotting and immnuno-histochemical analyses were conducted to determine the levels of VEGF, ICAM-1 and the transcriptional activators STAT3 (tyrosine-phosphorylated) and NF-kB (phosphorylated p65).
Treatment with trans-chalcone significantly inhibited RNV in the ischemic retina, as shown by decreased number of neovascular tufts. Trans-chalcone also blocked ischemia-induced VEGF and ICAM-1 expression and this effect correlated with trans-chalcone-mediated inhibition of activated STAT3 and NF-kB.
Our results show that trans-chalcone effectively prevents RNV in the murine retina thus suggesting that chalcone-derived flavonoids may be beneficial in preventing pathological neovascularization in the ischemic retina.
This PDF is available to Subscribers Only