Intravitreal injection of resveratrol inhibits laser-induced murine choroidal neovascularization

Hui-Ming Zhang1,2,3, Xiao-Hua Li4, Mingjiazi Chen5

  • 1Department of Dermatology, the Second Xiangya Hospital, Central South University, Changsha 410011, Hunan Province, China.

Abstract

Insights

Intravitreal resveratrol (RSV) effectively inhibits choroidal neovascularization (CNV) in mice by reducing endothelial cell migration and tube formation. This study demonstrates RSV

Area of Science:

  • Ophthalmology
  • Vascular Biology
  • Pharmacology

Background:

  • Choroidal neovascularization (CNV) is a leading cause of vision loss.
  • Current treatments for CNV have limitations.
  • Resveratrol (RSV) is a natural polyphenol with potential therapeutic properties.

Purpose of the Study:

  • To investigate the efficacy of intravitreal resveratrol (RSV) in a mouse model of laser-induced choroidal neovascularization (CNV).
  • To elucidate the underlying mechanisms of RSV's action on CNV development.

Main Methods:

  • Assessed RSV toxicity on choroidal endothelial cells (CECs) using MTT assay.
  • Evaluated RSV's impact on CEC migration and tube formation in vitro.
  • Induced CNV in mice via laser photocoagulation.
  • Quantified CNV inhibition using fluorescein angiography, confocal microscopy, and histology.
  • Analyzed vascular endothelial growth factor receptor 2 (VEGFR2) phosphorylation via immunostaining.

Main Results:

  • RSV showed no significant CEC toxicity at concentrations below 200 µmol/L.
  • RSV significantly inhibited VEGF-induced CEC migration and tube formation in vitro.
  • Intravitreal RSV administration markedly reduced laser-induced CNV formation, with significant reductions in leakage, volume, and area.
  • RSV treatment led to decreased phosphorylation of VEGFR2 in CNV lesions.

Conclusions:

  • Intravitreal resveratrol demonstrates a potent inhibitory effect on choroidal neovascularization.
  • RSV's anti-CNV mechanism involves the suppression of endothelial cell migration, tube formation, and VEGFR2 phosphorylation.
  • RSV holds promise as a therapeutic agent for treating CNV.

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