Abstract
Retinal neovascularization (RNV) is a critical pathological event and a major cause of blindness. Vascular inflammation and oxidative stress have been shown to play a key role in the induction and progression of RNV. Trans-Chalcone-derived flavonoids have been previously shown to be negative modulators of oxidative stress and inflammatory responses as well as tumor angiogenesis. In this study, we characterized the effects of the flavonoid trans-Chalcone in preventing RNV in a model of ischemic retinopathy. Ischemic retinopathy was induced in neonatal mice subjected to oxygen-induced retinopathy. Trans-Chalcone was administered intra-peritoneum at the dose of 25 mg/kg/day. Vascular density was assessed by morphometric analysis of flat mounted retinas stained with Texas red-Isolectin B4. Western blotting analysis was conducted to determine protein levels of vascular endothelial growth factor (VEGF), inter-cellular adhesion molecule 1 (ICAM-1) and the transcriptional activators' signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa beta (NF-κB). 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 inhibition of activated STAT3 and NF-κB. 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.
| Original language | English |
|---|---|
| Pages (from-to) | 350-354 |
| Number of pages | 5 |
| Journal | Experimental Eye Research |
| Volume | 93 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - Oct 2011 |
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Keywords
- Flavonoids
- Retinal neovascularization
- Trans-Chalcone
- Vascular endothelial growth factor
ASJC Scopus subject areas
- Ophthalmology
- Sensory Systems
- Cellular and Molecular Neuroscience
Cite this
Trans-Chalcone prevents VEGF expression and retinal neovascularization in the ischemic retina. / Lamoke, Folami; Labazi, Mohamed; Montemari, Annalisa; Parisi, Giovanni; Varano, Monica; Bartoli, Manuela.
In: Experimental Eye Research, Vol. 93, No. 4, 10.2011, p. 350-354.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Trans-Chalcone prevents VEGF expression and retinal neovascularization in the ischemic retina
AU - Lamoke, Folami
AU - Labazi, Mohamed
AU - Montemari, Annalisa
AU - Parisi, Giovanni
AU - Varano, Monica
AU - Bartoli, Manuela
PY - 2011/10
Y1 - 2011/10
N2 - Retinal neovascularization (RNV) is a critical pathological event and a major cause of blindness. Vascular inflammation and oxidative stress have been shown to play a key role in the induction and progression of RNV. Trans-Chalcone-derived flavonoids have been previously shown to be negative modulators of oxidative stress and inflammatory responses as well as tumor angiogenesis. In this study, we characterized the effects of the flavonoid trans-Chalcone in preventing RNV in a model of ischemic retinopathy. Ischemic retinopathy was induced in neonatal mice subjected to oxygen-induced retinopathy. Trans-Chalcone was administered intra-peritoneum at the dose of 25 mg/kg/day. Vascular density was assessed by morphometric analysis of flat mounted retinas stained with Texas red-Isolectin B4. Western blotting analysis was conducted to determine protein levels of vascular endothelial growth factor (VEGF), inter-cellular adhesion molecule 1 (ICAM-1) and the transcriptional activators' signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa beta (NF-κB). 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 inhibition of activated STAT3 and NF-κB. 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.
AB - Retinal neovascularization (RNV) is a critical pathological event and a major cause of blindness. Vascular inflammation and oxidative stress have been shown to play a key role in the induction and progression of RNV. Trans-Chalcone-derived flavonoids have been previously shown to be negative modulators of oxidative stress and inflammatory responses as well as tumor angiogenesis. In this study, we characterized the effects of the flavonoid trans-Chalcone in preventing RNV in a model of ischemic retinopathy. Ischemic retinopathy was induced in neonatal mice subjected to oxygen-induced retinopathy. Trans-Chalcone was administered intra-peritoneum at the dose of 25 mg/kg/day. Vascular density was assessed by morphometric analysis of flat mounted retinas stained with Texas red-Isolectin B4. Western blotting analysis was conducted to determine protein levels of vascular endothelial growth factor (VEGF), inter-cellular adhesion molecule 1 (ICAM-1) and the transcriptional activators' signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa beta (NF-κB). 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 inhibition of activated STAT3 and NF-κB. 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.
KW - Flavonoids
KW - Retinal neovascularization
KW - Trans-Chalcone
KW - Vascular endothelial growth factor
UR - http://www.scopus.com/inward/record.url?scp=80055038350&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=80055038350&partnerID=8YFLogxK
U2 - 10.1016/j.exer.2011.02.007
DO - 10.1016/j.exer.2011.02.007
M3 - Article
C2 - 21354136
AN - SCOPUS:80055038350
VL - 93
SP - 350
EP - 354
JO - Experimental Eye Research
JF - Experimental Eye Research
SN - 0014-4835
IS - 4
ER -