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Updated: Jun 20, 2026
A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure
Published on: July 14, 2016
[Erythropoietin protects retinal ganglion cells and visual function after ocular ischemia and optic nerve
T Jehle1, W Meschede, R Dersch
1Augenklinik des Klinikums der Albert-Ludwigs-Universität Freiburg i.Br., Killianstrasse 5, 79106, Freiburg i.Br. tomjeh@googlemail.com
Background:
The glycoprotein erythropoietin (EPO) has been shown to be protective in models of neuronal disease and reduced apoptosis of retinal ganglion cells (RGC) after transection of the optic nerve and in glaucoma. In this study we assessed in vivo the properties of EPO on survival of RGC after ischemia and optic nerve compression, as well as on postischemic visual function. Furthermore, the safety of intravitreal injection was assessed.
Methods:
In all experiments, EPO was administered intravitreally in male Brown Norway rats. Ocular ischemia was induced by elevating the intraocular pressure for 55 min. The calibrated optic nerve compression was performed for 10 s. RGC were marked stereotactically and quantified by fluorescence microscopy. The retinal function was quantified by electroretinography (ERG) and the whole visual pathway by visual evoked potential (VEP).
Results:
EPO (2 and 20 units per eye, n=9-21) increased the survival of RGC after ischemia by 21+/-21% and 127+/-31% (mean +/- SEM) and after optic nerve compression by 28+/-12% and 58+/-13%. With EPO (20 units), postischemic function was increased, in ERG by 71+/-13% (a-wave) and 75+/-19% (b-wave) and in VEP by 264+/-65% (p=0.053). Neither the ERG parameters, nor the VEP, nor the number of RGC differed significantly after intravitreal injection of EPO (5, 50, and 200 units, n=6-7) in healthy eyes.
Conclusion:
The combination of toxicological safety and protection of retinal neurons makes EPO a promising drug for ischemic retinal diseases and traumatic optic neuropathy.
