Background  Intracerebral hemorrhage is characterized by high morbidity, disability and mortality. Inflammation after intracerebral hemorrhage is an impotant factor causing secondary brain injury and affects the prognosis of patients. Astaxaanthin has biological effects such as anti-inflammatary and anti-oxidation, and can cross the blood-brain barrier, with a neuroprotective effect on a variety of nervous system diseases.

  Objective  To observe the effects of astaxanthin (ASX) against microglial cell activation in rats with intracerebral hemorrhage.

  Methods  A total of 64 Sprague-Dawley male rats were randomly divided into sham-operation group, intracerebral hemorrhage (ICH) group, ASX low dose group (20 mg/kg) and ASX high dose group (40 mg/kg) of equal number with random number table. Autologous blood was injected into caudate nucleus to establish ICH model. Feeding ASX low dose group and ASX high dose group with corresponding dose of ASX by gavage, the other groups were given the same volume of peanut oil. We assessed rats in each group by the neurological severity scores (NSS) at 3d and observed the pathological change of brain tissue structure by hematoxylin-eosin staining (HE staining), and the water content of brain tissue (BWC) was measured by dry-wet weight method and the expressions of Iba-1, NF-κ B protein were detected by immunofluorescence or Western blotting. The levels of IL-1β, TNF-α in brain tissue were detected by ELISA.

  Results  Compared with the sham-operation group, the score of NSS decreased significantly (17.44 ± 0.89 vs 7.56 ± 1.55, P＜0.05), while the water content of ICH group's brain tissue increased (77.72% ± 0.89% vs 84.60% ± 0.90%, P＜0.05). HE staining of the ICH group showed large area of necrosis around the brain hematoma tissue, and cells swelled, dissolved and degeneration around the lesions. The expression level of NF-κ B (0.092 ± 0.020 vs 0.595 ± 0.028), TNF-α (134.83 ± 15.04 pg/mL vs 781.20 ± 100.29 pg/mL), IL-1β (170.19 ± 13.19 pg/mL vs 655.11 ± 61.98 pg/mL) in ICH group were significantly higher than those in the sham-operation group (all P＜0.05). Compared with the ICH group, the MSS score of the ASX low dose group and the ASX high dose group (9.5 ± 1.46 and 10.75 ± 1.69 vs 7.56 ± 1.55, P＜0.05) improved significantly, and the pathological changes reduced, while the brain water content decreased significantly (82.43% ± 0.52% and 81.04% ± 0.98% vs 84.60% ± 0.90%, P＜0.05). The expression level of NF-κ B (0.479 ± 0.03 and 0.387 ± 0.031 vs 0.595 ± 0.028), TNF-α (445.40 ± 66.34 pg/mL and 346.66 ± 39.13 pg/mL vs 781.20 ± 100.29 pg/mL) and IL-1β (456.99 ± 52.83 pg/mL and 331.46 ± 30.90 pg/mL vs 655.11 ± 61.98 pg/mL) were down regulated (all P＜0.05).

  Conclusion  ASX may inhibit microglial cell activation and cytokine production to reduce the inflammatory reaction, alleviate the extent of brain edema, which has a positive effect on neuroprotective for rats after ICH.