Astragalus root extract inhibits retinal cell apoptosis and repairs damaged retinal neovascularization in retinopathy of prematurity

Cell Cycle. 2019 Nov;18(22):3147-3159. doi: 10.1080/15384101.2019.1669998. Epub 2019 Sep 29.

Abstract

Since the functions of Astragalus root extract in retinopathy remain to be unraveled, this study is performed to elucidate whether Astragalus root extract functions in retinal cell apoptosis and angiogenesis in retinopathy of prematurity (ROP). Newborn mice were selected for establishing mice models of oxygen-induced retinopathy (OIR), which were treated with high-, medium- or low-Astragalus root extract. Evans Blue (EB) was perfused to detect the blood retinal barrier. Additionally, the vascular morphology, number of endothelial cell nuclei of neovascularization, proliferation of blood vessels, ultrastructural changes were determined via a series of assays. Moreover, levels of reactive oxygen species (ROS), expression of other factors such as VEGF, PEDF, IGF-1, HIF-1α, Bax, Bcl-2, eNOS, nNOS, and iNOS were detected. Astragalus root extract was found to protect blood-retinal barrier in the OIR model mice through repairing the structure and morphology of retina, inhibiting ROS production, retinal cell apoptosis, as well as improving retinal vascular angiogenesis. Astragalus root extract was also found to decrease VEGF and HIF-1α expression, but enhance PEDF and IGF-1 expression in the OIR model mice, thereby protecting retinas in ROP. This study highlights that Astragalus root extract is able to suppress retinal cell apoptosis and repair damaged retinal neovascularization in ROP, which provides basis for ROP therapy.

Keywords: Astragalus root extract; oxygen induced retinopathy; retinopathy of prematurity.

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Astragalus Plant / chemistry*
  • Disease Models, Animal
  • Endothelial Cells / metabolism
  • Endothelial Cells / ultrastructure
  • Eye Proteins / genetics
  • Eye Proteins / metabolism
  • Hypoxia-Inducible Factor 1, alpha Subunit / genetics
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • Insulin-Like Growth Factor I / genetics
  • Insulin-Like Growth Factor I / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Microscopy, Electron
  • Neovascularization, Pathologic / drug therapy*
  • Neovascularization, Pathologic / metabolism
  • Nerve Growth Factors / genetics
  • Nerve Growth Factors / metabolism
  • Nitric Oxide Synthase Type I / genetics
  • Nitric Oxide Synthase Type I / metabolism
  • Nitric Oxide Synthase Type II / genetics
  • Nitric Oxide Synthase Type II / metabolism
  • Nitric Oxide Synthase Type III / genetics
  • Nitric Oxide Synthase Type III / metabolism
  • Oxygen / toxicity
  • Plant Extracts / pharmacology
  • Plant Extracts / therapeutic use*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Reactive Oxygen Species / metabolism
  • Retina / cytology
  • Retina / drug effects*
  • Retina / pathology
  • Retina / ultrastructure
  • Retinal Vessels*
  • Retinopathy of Prematurity / chemically induced
  • Retinopathy of Prematurity / drug therapy*
  • Retinopathy of Prematurity / genetics
  • Retinopathy of Prematurity / metabolism*
  • Serpins / genetics
  • Serpins / metabolism
  • Vascular Endothelial Growth Factor A / genetics
  • Vascular Endothelial Growth Factor A / metabolism
  • bcl-2-Associated X Protein / metabolism

Substances

  • Bax protein, mouse
  • Eye Proteins
  • Hif1a protein, mouse
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Nerve Growth Factors
  • Plant Extracts
  • Proto-Oncogene Proteins c-bcl-2
  • Reactive Oxygen Species
  • Serpins
  • Vascular Endothelial Growth Factor A
  • bcl-2-Associated X Protein
  • pigment epithelium-derived factor
  • Insulin-Like Growth Factor I
  • Nitric Oxide Synthase Type I
  • Nitric Oxide Synthase Type II
  • Nitric Oxide Synthase Type III
  • Nos1 protein, mouse
  • Nos2 protein, mouse
  • Nos3 protein, mouse
  • Oxygen

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