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