May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
The Neuroprotective Role of Hyperbaric Oxygen Chamber Therapy in Ischemic Optic Neuropathy in a Murine Model
Author Affiliations & Notes
  • S. Dadon
    The Krieger Eye Research Laboratory, Felsenstein Medical Research Center, Petah Tiqwa, Israel
    The Mina and Everard Goodman, Faculty of Life Sciences, Bar Ilan University, Ramat Gan, Israel
  • M. Hasanreisoglu
    Department of Ophthalmology, Rabin Medical Center, Petah Tiqwa, Israel
  • D. Weinberger
    Department of Ophthalmology, Rabin Medical Center, Petah Tiqwa, Israel
    Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel
  • N. Goldenberg-Cohen
    The Krieger Eye Research Laboratory, Felsenstein Medical Research Center, Petah Tiqwa, Israel
    Department of Ophthalmology, Rabin Medical Center, Petah Tiqwa, Israel
  • Footnotes
    Commercial Relationships  S. Dadon, None; M. Hasanreisoglu, None; D. Weinberger, None; N. Goldenberg-Cohen, None.
  • Footnotes
    Support  The Zanvyl and Isabelle Krieger Fund, Baltimore, Maryland, USA
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 4939. doi:https://doi.org/
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      S. Dadon, M. Hasanreisoglu, D. Weinberger, N. Goldenberg-Cohen; The Neuroprotective Role of Hyperbaric Oxygen Chamber Therapy in Ischemic Optic Neuropathy in a Murine Model. Invest. Ophthalmol. Vis. Sci. 2008;49(13):4939. doi: https://doi.org/.

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

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Abstract

Purpose: : To investigate the effect of hyperbaric oxygen (HBO) chamber treatment of anterior ischemic optic neuropathy (AION) in mice.

Methods: : AION was induced in one eye of 55 mice by laser activation of intravenously injected rose-Bengal. The fellow eye was untreated and served as an internal control. Twenty-eight mice were exposed to 100% oxygen (2 Atm) for 90 minutes immediately following injury and daily thereafter for up to 14 days. Retinas were harvested at 1, 3 and 21 days after AION induction, and mRNA levels of SOD-1, HO-1, eNOS and Thy-1 were analyzed using quantitative real-time polymerase chain reaction. Histological analysis of retinal sections was performed as well.

Results: : At 1 day following AION induction, expression of the oxidative-stress-induced gene, SOD-1, decreased to 82% of control levels. At 3 days, expression of the ischemia-related genes, HO-1 and eNOS, decreased to 74% of control levels. At 21 days, HO-1 rose to 2.2-fold of control levels, whereas eNOS decreased to 48% of controls. Treatment with HBO prevented the decrease in SOD-1 expression on 1 day and was associated with an increase in HO-1 and eNOS on day 3. At 21 days after treatment, SOD-1 decreased whereas eNOS increased. HO-1 increased to a lower level than without treatment. The HBO-treated animals did not show retinal ganglion cell loss or a decrease in Thy-1 expression compared to the untreated mice.

Conclusions: : HBO treatment after AION induction in mice influences the expression levels of oxidative-stress and ischemia-related genes and may exert a neuroprotective effect in this setting.

Keywords: retina • gene/expression 
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