PURPOSE: 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.
PURPOSE: 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: Kurtuluş Açiksari; Seracettin Eğin; Gülçin Hepgül; Bengüsu Mirasoğlu; Gamze Tanriverdi; Devrim S Kanber; Sibel Demirci; Halil Doğan; Doğaç N Özüçelik; Akın S Toklu; İsmail Seçkin; Hakan T Yanar Journal: Diving Hyperb Med Date: 2019-12-20 Impact factor: 0.887
Authors: Tu Hu; Qiuting You; Dan Chen; Jianbin Tong; Lei Shang; Jia Luo; Yi Qiu; Huimin Yu; Leping Zeng; Jufang Huang Journal: Neurochem Res Date: 2016-01-30 Impact factor: 3.996
Authors: Ana Sofia Lopes; Rita Basto; Susana Henriques; Luísa Colaço; Filomena Costa E Silva; Isabel Prieto; Francisco Guerreiro Journal: Case Rep Ophthalmol Med Date: 2019-12-28