Abstract

Objective To study the effects of astaxanthin (ATX) on the early brain injury (EBI) after experimental subarachnoid hemorrhage (SAH) in rats.Methods A total of 72 male SD rats were randomly divided into three groups:sham group,SAH + vehicle group and SAH + ATX group.The prechiasmatic cistern SAH rat model was established in this experiment.Brain edema and Evans blue extravasation were measured at 24 h after surgery.The levels of Caspase-3,apoptotic index and malondialdehyde (MDA),glutathione (GSH),and superoxide dismutase (SOD) in the brain cortex were evaluated by Western blotting,terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining,and spectrophotometric method,respectively.Results The brain edema [(80.76 ± 0.67) %] and blood-brain barrier permeability [(2.17 ±0.53) μg/g] were significantly aggravated at 24 h after SAH.In addition,the levels of Caspase-3 expression [(0.49 ± 0.13)] and neural cell apoptosis [(41.54 ±9.38) %] were increased in the inferior basal temporal lobe followomh SAH.After ATX administration,the brain edema [(79.91 ± 0.42) %],BBB disruption [(1.35 ± 0.46) μg/g],Caspase-3 levels [(0.34 ± 0.06)] and neural cell apoptosis [(27.86 ± 5.17) %] were ameliorated after SAH.Meanwhile,ATX could attenuate the oxidative stress injury [(MDA:2.52 ± 0.60,4.44 ± 1.32 and 2.64 ±0.78); (GSH:6.50±1.80,3.72±1.12 and 6.23 ±0.87); (SOD:25.71 ±4.00,14.71 ±2.35 and 21.61 ± 3.87)] in brain cortex after SAH.Conclusion ATX could alleviate EBI after SAH by its powerful anti-oxidant property. Key words: Subarachnoid hemorrhage; Early brain injury; Astaxanthin; Oxidative stress injury

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