June 2021
Volume 62, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2021
The neuroprotective effect of propranolol against retinal degeneration in a mouse model of light injury.
Author Affiliations & Notes
  • Clayton Kirk
    Ophthalmology, Loyola University Chicago, Maywood, Illinois, United States
  • ZHIQUN TAN
    University of California Irvine, Irvine, California, United States
  • James F. McDonnell
    Ophthalmology, Loyola University Chicago, Maywood, Illinois, United States
  • Jay Perlman
    Ophthalmology, Loyola University Chicago, Maywood, Illinois, United States
  • Ping Bu
    Ophthalmology, Loyola University Chicago, Maywood, Illinois, United States
  • Footnotes
    Commercial Relationships   Clayton Kirk, None; ZHIQUN TAN, None; James McDonnell, None; Jay Perlman, None; Ping Bu, None
  • Footnotes
    Support  Illinois Society for the Prevention of Blindness
Investigative Ophthalmology & Visual Science June 2021, Vol.62, 2724. doi:
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      Clayton Kirk, ZHIQUN TAN, James F. McDonnell, Jay Perlman, Ping Bu; The neuroprotective effect of propranolol against retinal degeneration in a mouse model of light injury.. Invest. Ophthalmol. Vis. Sci. 2021;62(8):2724.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Age related macular degeneration (AMD) is the leading cause of vision loss in developed countries. Propranolol is a commonly used, nonspecific β12 adrenergic receptor antagonist (BARA) that has been shown to have a neuroprotective effect on various mouse retinal injury models. We hypothesize that systemic propranolol will exhibit a protective effect against retinal degeneration in the mouse model and has potential to protect from vision loss related to AMD in the future.

Methods : BALB/c albino mice were divided into 2 groups: vehicle-treated mice and propranolol treated. Light injury mice were exposed to 8,000 lux-cool, white, fluorescent light for 2 hours to induce light injury. Vehicle (4% v/v citrate buffer in normal saline) or propranolol (20 mg/kg/dose freshly prepared in normal saline solution before injection, stock solution at 50mg/ml in citrate buffer) was injected subcutaneously following light injury for 4 days. Scotopic electroretinography (ERG) was recorded before light injury and 5 days following light injury.

Results : Following retinal light injury, ERG a- and b-wave amplitudes were significantly reduced in the control mice. Propranolol treatment significantly attenuated light-induced loss of retinal function as compared to control treated mice. Before treatment, scotopic ERG a- and b-wave amplitudes were an average of 347.9 μV and 616.4 μV, respectively, in the control group and 368.6 μV and 618.9 μV, respectively, in the propranolol treatment group. Following retinal light injury, ERG a-wave amplitudes were 71.75 μV in the control group and 161.2 μV in the propranolol treatment group (p < 0.01). Following retinal light injury, ERG b-wave amplitudes were 142.4 μV in the control group and 360.2 μV in the propranolol treatment group (p < 0.01).

Conclusions : Propranolol treatment of mice demonstrated a substantial effect on preserving ERG a- and b-wave amplitudes following retinal light injury as compared to a control group. These initial findings suggest that propranolol may represent a novel therapy for retinal degenerative conditions.

This is a 2021 ARVO Annual Meeting abstract.

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