Abstract
BackgroundIncreasing experimental and clinical data indicate that early brain injury (EBI) after subarachnoid hemorrhage (SAH) largely contributes to unfavorable outcomes, and it has been proved that EBI following SAH is closely associated with oxidative stress and brain edema. The present study aimed to examine the effect of hydrogen, a mild and selective cytotoxic oxygen radical scavenger, on oxidative stress injury, brain edema and neurology outcome following experimental SAH in rabbits.ResultsThe level of MDA, caspase-12/3 and brain water content increased significantly at 72 hours after experimental SAH. Correspondingly, obvious brain injury was found in the SAH group by terminal deoxynucleotidyl transferase-mediated uridine 5’-triphosphate-biotin nick end-labeling (TUNEL) and Nissl staining. Similar results were found in the SAH + saline group. In contrast, the upregulated level of MDA, caspase-12/3 and brain edema was attenuated and the brain injury was substantially alleviated in the hydrogen treated rabbits, but the improvement of neurology outcome was not obvious.ConclusionThe results suggest that treatment with hydrogen in experimental SAH rabbits could alleviate brain injury via decreasing the oxidative stress injury and brain edema. Hence, we conclude that hydrogen possesses the potential to be a novel therapeutic agent for EBI after SAH.
Highlights
Increasing experimental and clinical data indicate that early brain injury (EBI) after subarachnoid hemorrhage (SAH) largely contributes to unfavorable outcomes, and it has been proved that EBI following SAH is closely associated with oxidative stress and brain edema
The appetite scores of the rabbits in the SAH + hydrogen-rich saline group were lower than those observed in the SAH group, but the difference was not statistically significant (P > 0.05, data not shown)
After the two-time injection of blood, all the SAH models were qualified: obvious blood clot can be seen around the brain stem and in the basal cisterns in each of the rabbits 3 days after induced SAH
Summary
Increasing experimental and clinical data indicate that early brain injury (EBI) after subarachnoid hemorrhage (SAH) largely contributes to unfavorable outcomes, and it has been proved that EBI following SAH is closely associated with oxidative stress and brain edema. The present study aimed to examine the effect of hydrogen, a mild and selective cytotoxic oxygen radical scavenger, on oxidative stress injury, brain edema and neurology outcome following experimental SAH in rabbits. Little success has been achieved in improving outcome following SAH [5,6]. This idea has recently been challenged by the failure of the drug clazosentan to improve patients’ outcome, despite reversing vasoconstriction [6,7]. We propose to look beyond vasoconstriction, and consider more factors, such as ischemia, disruption of the blood–brain barrier, activation of apoptotic and inflammatory pathways, and cortical spreading depression in the early stage following SAH [8,9]
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