Table 1 Summary of neurological outcomes in acute focal brain ischemia NBO studies that measure oxidative stress

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 % O_2; 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 cNBO^a

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]