title: Reduction of apoptosis in ischemic retinas of two mouse models using hyperbaric oxygen treatment.
abstract: OBJECTIVE
  To investigate the effect of hyperbaric oxygen (HBO) chamber treatment in mouse models of retinal ischemia.
  
  
  METHODS
  Unilateral central retinal artery occlusion (CRAO) or optic nerve crush (ONC) was induced in 50 mice each, of which 30 were treated with 100% oxygen at 2 atm for 90 minutes immediately after injury and then daily for up to 14 days. Mice were euthanatized on days 1, 3, and 21 for histologic analysis, apoptosis assay, and quantitative real-time polymerase chain reaction test. Findings were analyzed by injury and by treatment.
  
  
  RESULTS
  HBO treatment reduced cell loss from 58% to 30% in the CRAO model and from 52% to 32% in the ONC model. In both models, it was associated with significantly increased cell survival in the retinal ganglion cell layer. Expression levels of the proapoptosis genes (bax, caspase-3) decreased minimally in the HBO-treated CRAO mice on day 1, but this trend was reversed on day 3. In the ONC group, levels of caspase-3, bax, and bcl-x increased on day 1 and dropped below baseline on day 3. The pattern of changes in the expression levels of the ischemia- and oxidative-stress-related genes (HO-1, SOD-1, GPX-1, NOX-2) and the effectiveness of HBO treatment varied by model. Overall, however, gene expression levels that increased in the untreated mice increased further with HBO treatment and levels that decreased, decreased further with treatment.
  
  
  CONCLUSIONS
  HBO treatment protects injured neuronal cells from apoptosis. Response to treatment differs molecularly after ONC or CRAO. These results should prompt clinical trials of acute ischemic retinal damage.
authors.affiliation: Krieger Eye Research Laboratory, Felsenstein Medical Research Center, Petah Tiqwa, Israel.
authors.forename: Vera
authors.initials: V
authors.lastname: Gaydar
authors.forename: David
authors.initials: D
authors.lastname: Ezrachi
authors.forename: Olga
authors.initials: O
authors.lastname: Dratviman-Storobinsky
authors.forename: Shir
authors.initials: S
authors.lastname: Hofstetter
authors.forename: Bat Chen R
authors.initials: BC
authors.lastname: Avraham-Lubin
authors.forename: Nitza
authors.initials: N
authors.lastname: Goldenberg-Cohen
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D002470:Cell Survival; D004195:Disease Models, Animal; D006931:Hyperbaric Oxygenation; D020287:In Situ Nick-End Labeling; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009409:Nerve Crush; D018917:Optic Neuropathy, Ischemic / Q000235:genetics / Q000378:metabolism / Q000628:therapy*; D018384:Oxidative Stress; D060888:Real-Time Polymerase Chain Reaction; D015356:Retinal Artery Occlusion / Q000209:etiology; D012164:Retinal Diseases / Q000235:genetics / Q000378:metabolism / Q000628:therapy*; D012165:Retinal Ganglion Cells / Q000502:physiology*; D012171:Retinal Vessels; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism; D051020:bcl-X Protein / Q000235:genetics / Q000378:metabolism
chemical_list: C494812:Bcl2l1 protein, mouse; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein; C505409:Casp3 protein, mouse; D053148:Caspase 3