July 2019
Volume 60, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2019
Neuroprotective effects via hypothermia on hydrogen peroxide damaged porcine retinae
Author Affiliations & Notes
  • Stephanie C Joachim
    Experimental Eye Research Institute, Ruhr-University Bochum, Bochum, Germany
  • Ana Maliha
    Experimental Eye Research Institute, Ruhr-University Bochum, Bochum, Germany
  • Sven Grauthoff
    Experimental Eye Research Institute, Ruhr-University Bochum, Bochum, Germany
  • Sandra Kuehn
    Experimental Eye Research Institute, Ruhr-University Bochum, Bochum, Germany
  • Jose Hurst
    Centre for Ophthalmology Tuebingen, University Eye Hospital Tuebingen, Tuebingen, Germany
  • Hannah Doepper
    Experimental Eye Research Institute, Ruhr-University Bochum, Bochum, Germany
  • Sven Schnichels
    Centre for Ophthalmology Tuebingen, University Eye Hospital Tuebingen, Tuebingen, Germany
  • Footnotes
    Commercial Relationships   Stephanie Joachim, None; Ana Maliha, None; Sven Grauthoff, None; Sandra Kuehn, None; Jose Hurst, None; Hannah Doepper, None; Sven Schnichels, None
  • Footnotes
    Support  set Stiftung (Germany)
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 5721. doi:
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      Stephanie C Joachim, Ana Maliha, Sven Grauthoff, Sandra Kuehn, Jose Hurst, Hannah Doepper, Sven Schnichels; Neuroprotective effects via hypothermia on hydrogen peroxide damaged porcine retinae. Invest. Ophthalmol. Vis. Sci. 2019;60(9):5721.

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

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Abstract

Purpose : Hydrogen peroxide (H2O2) can be used in vitro to simulate oxidative stress, causing a strong neurodegeneration of the inner retinal layers. Oxidative stress plays an important role in the development of retinal diseases, including glaucoma and ischemia. Thus, we investigated, whether processes underlying oxidative stress can be prevented by hypothermia using an ex vivo organ culture model of porcine retina.

Methods : Porcine retinal explants were cultivated for eight days. Oxidative stress was induced via 300 µM H2O2 on day one for three hours. Hypothermia treatment, at 30°C, was applied simultaneously. Retinal ganglion cells (RGCs), bipolar, cholinergic amacrine cells, and microglia were evaluated immunohistologically followed by cell counts and statistical analysis.

Results : A significant RGC loss was seen in the H2O2 group (32.6±4.2%) in comparison to the control group (100.0±3.6%; p<0.001). Nearly 30% of the RGCs were rescued through hypothermia (66.9±3.4%), leading to a higher number of RGCs than in the H2O2 group (p<0.001). In addition, more apoptotic RGCs were detected in the H2O2 group (201.1±20.6%) in comparison to controls (100.0±14.2%; p<0.001). Hypothermia prevented apoptotic mechanisms (100.4±4.2%) in comparison to the H2O2 group (p<0.001). Also, cholinergic amacrine cells (p=0.048) and microglia (p<0.001) were protected from the damaging effects due to H2O2. Rod bipolar cells were the only cell type that was not preserved by hypothermia.

Conclusions : H2O2 induces strong degeneration processes in porcine retinae by mimicking oxidative stress. The damaging effect of H2O2 to the retinal cells were totally counteracted by hypothermia. Especially retinal ganglion cells were protected.

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.

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