4.5 Article

Hyperbaric Oxygen Preconditioning Promotes Survival of Retinal Ganglion Cells in a Rat Model of Optic Nerve Crush

期刊

JOURNAL OF NEUROTRAUMA
卷 27, 期 4, 页码 763-770

出版社

MARY ANN LIEBERT, INC
DOI: 10.1089/neu.2009.1005

关键词

hyperbaric oxygen preconditioning; neuroprotection; optic nerve crush; retinal ganglion cells

资金

  1. National Basic Research Program of China [2005CB724302]

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In this study we tested the hypothesis that hyperbaric oxygen preconditioning (HBO-PC) reduces retinal neuronal death due to optic nerve crush (ONC). Adult male Sprague-Dawley rats were subjected to ONC accompanied by a contralateral sham operation. HBO-PC was conducted four times by giving 100% oxygen at 2.5 atmospheres absolute (ATA) for 1 h every 12 h for 2 days prior to ONC. The rats were euthanized at 1 or 2 weeks after ONC. Retinal ganglion cell (RGC) density was counted by hematoxylin and eosin (H&E) staining of the retina and retrograde labeling with FluoroGold application to the superior colliculus. Visual function was assessed by flash visual evoked potentials (FVEP). TUNEL straining and caspase-3 and caspase-9 activity in the retinas were assessed. The RGC density in the retinas of ONC HBO-PC-treated rats was significantly higher than that of the corresponding ONC-only rats (the survival rate was 67.2% versus 49.7% by H&E staining, and 60.3% versus 28.9% by retrograde labeling with FluoroGold, respectively; p < 0.01) at 2 weeks after ONC. FVEP measurements indicated a significantly better preserved latency and amplitude of the P1 wave in the ONC HBO-PC-treated rats than the ONC-only rats (92 +/- 7 msec, 21 +/- 3 mu v in the sham-operated group, 117 +/- 12 msec, 14 +/- 2 mu v in the HBO-PC-treated group, and 169 +/- 15 msec, 7 +/- 1 mu v in the corresponding ONC group; p < 0.01). TUNEL assays showed fewer apoptotic cells in the HBO-PC-treated group, accompanied by the suppression of caspase-3 and caspase-9 activity. These results demonstrate that HBO-PC appears to be neuroprotective against ONC insult via inhibition of neuronal apoptosis pathways.

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