Table 1.
Summary of neurological outcomes in acute focal brain ischemia NBO studies that measure oxidative stress
| Model | NBO intervention | Oxidative stress results | Neurological outcome results | Ref. |
|---|---|---|---|---|
| MCAO (2 h) and reperfusion (60 min ) in rats | NBO (100 % O2) during MCAO and reperfusion | NBO did not increase HO-1 induction and protein carbonyl formation (no significant differences between groups) | NBO significantly reduced total infarct volume (70 %) and cortex infarct volume (92 %), but not significantly in the striatum. No significant differences in BBB damage. | [12] |
| MCAO (1,2,3, or 4 h) in rats | NBO (100 % O2) during MCAO | NBO did not increase markers for O2·− generation (Het) (no significant differences between groups) | NBO groups improved neurological scores and had significantly smaller infarct volumes after 1,2, and 3 h MCAO | [14] |
| MCAO (90 min) and reperfusion (90 min) in rats | dNBO (95 % O2) during MCAO or rNBO during reperfusion | dNBO (not rNBO) significantly reduced 8-OHdG production. dNBO and rNBO did not affect O2·− generation (Het). | NBO during MCAO significantly reduced infarct volume (40 %). NBO during reperfusion reduced infarction volume (15 %: not significant) | [17] |
| MCAO (90 min) and reperfusion (22.5 h) in WT and gp91phox-KO mice | NBO (95 % O2) during MCAO | NBO significantly inhibited gp91phox expression, NADPH oxidase activity, and MMP-9 induction in WT | NBO treatment and gp91phox-KO significantly reduced BBB damage. Inhibition of gp91phox may be an important mechanism underlying NBO-afforded BBB protection | [23] |
| MCAO (90 min) and reperfusion (90 min) in mice | dNBO (100 % O2) during MCAO or rNBO (100 %) during reperfusion | dNBO significantly decreased levels of 4HNE, NT, 8-OHdG oxidation. No significant differences with rNBO | dNBO significantly reduced infarct volume (~50 %) and improved sensorimotor scores. rNBO worsened the ischemic lesion, but no significant difference in sensorimotor scores | [27] |
| BCAO (15 min) and blood pressure (50 mmHg) reduction in rats | NBO (100 % O2; 3 h) after BCAO | NBO did not lead to enhanced H2O2 or ROS production (no significant differences between groups) | No significant differences in caudoputaminal and neocortical damaged neurons score or percent of hippocampal necrotic neurons | [32] |
| MCAO (90 min) and reperfusion (22.5 h) in rats | NBO (95 % O2) given during MCAO | NBO significantly inhibited gp91phox expression and NADPH oxidase activity | NBO significantly reduced MRI ADC lesion volume (37 %) | [67] |
| MCAO (90 min) and reperfusion (22.5 h) in rats | iNBO (100 % O2), sNBO, nNBO, or cNBOa | iNBO and nNBO groups significantly decreased O2·− production (Het) | iNBO significantly reduced infarct volume (34 %) equivalent to nNBO. sNBO did not decrease infarct volume and cNBO did not improve protection over iNBO or nNBO | [69] |
| MCAO (90 min) and reperfusion (22.5 h) in rats | NBO (100 % O2) given for 2,4 or 8 h 30 min after MCAO | NBO (2,4 and 8 h) significantly reduced 8-OHdG and gp91phox production (greatest reduction with 8 h NBO) | NBO (2,4 and 8 h) significantly reduced total infarct volume and infarct volume in the cortex and subcortex (8 h NBO offered the greatest efficacy) | [70] |
| MCAO (90 min) and reperfusion (22.5 h) in rats | NBO (95 % O2) given during MCAO | NBO significantly inhibited gp91phox expression, NADPH oxidase activity, and MMP-9 induction | NBO significantly decreased BBB permeability coefficient (MRI) and brain edema | [71] |
| MCAO (90 min) in WT and SOD2-KO mice | NBO (100 % O2) (60 min) started 25 min after MCAO | NBO significantly decreased O2·− generation (Het) in WT mice. | NBO does not affect infarct size in SOD2-KO mice and the effect of NBO on infarct size in WT mice was not presented | [72] |
| MCAO (10,30,60 or 90 min) in rats | NBO (95 % O2) given during MCAO | NBO significantly delayed and attenuated ·NO production (NOx−:nitrite plus nitrate) and significantly reduced 3-NT formation | NBO significantly decreased total infarct volume, particularly in the cortex, but not significantly in the striatum | [73] |
MCAO middle cerebral artery occlusion, HO-1 heme oxygenase-1, O 2 · − superoxide, Het dihydroethidium, dNBO during MCAO, rNBO during reperfusion, 4HNE 4-hydroxynonenal, NT nitrotyrosine, 8-OHdG 8-hydroxy-2′–deoxyguanosine, BCAO bilateral carotid artery occlusion, WT wild-type, KO knock-out, iNBO Intermittent, sNBO Short, nNBO normal or continuous, cNBO combination, ·NO nitric oxide
a see reference for details