Acute cerebral infarction (ACI) is susceptible to cause disability or death of people. Astaxanthin (ATX) possesses the protective effect of organ injury. Therefore, the study was to explore the potential mechanism of protective effect with ATX on ACI.

30 SD rats were divided into Sham, ACI, and ATX groups. The rats in the ATX group were pretreated with ATX by gavage for three days before surgery, while the rats in the other two groups were pretreated with saline. The model of ACI was established by thread embolization. 24 h after the operation, the neurological function was scored, and cerebral infarct area and pathological morphology of brains were measured; the edema of the brain was detected by dry/wet method; Western blot was applied to measure the translocation of Nrf-2 and the protein expression of HO-1, Bax and BCL-2; Brain cell apoptosis was assessed through TUNEL; ELISA was used to detect the oxidative stress factors of catalase (CAT) superoxide dismutase (SOD), glutathione peroxidase (GPX) and malondialdehyde (MDA), and the inflammatory factors of TNF-α, IL-1β, IL-6.

Compared with the ACI group, ATX pretreatment can significantly improve neurological function; reduce the edema index of the brain, cerebral infarct area, cerebral pathological damage and apoptosis of brain cells. Moreover, ATX also can increase the protein expression of nuclear Nrf-2, HO-1, BCL-2, CAT, SOD, and GPX by decreasing the content of TNF-α, IL-1β, IL-6, MDA, Bax and cytosolic Nrf-2.

ATX might have a protective effect of acute cerebral infarction, and the mechanism is probably associated with suppressing oxidative stress, inflammation, and apoptosis by activating Nrf-2/HO-1signalling.