Xingfen Su, Lijin Wu, Fuxiang Chen
Astaxanthin (ATX) is a dietary carotenoid that possesses potent effects of anti-oxidation, anti-inflammation, and anti-cell death. ATX has neuroprotective properties in a variety of neurological diseases. However, whether ATX has a neuroprotective effect in intracerebral hemorrhage (ICH) is still unknown. The present study was carried out to explore the protective effects of ATX and the underlying mechanisms using a collagenase-induced ICH in mice. Single dose of astaxanthin (100 mg/kg) or vehicle was administrated to mice through intraperitoneal injection at 30 min after ICH induction. Our results showed that ATX significantly ameliorated secondary brain injury after ICH, including neurological deficits, neural cell degeneration, blood-brain barrier (BBB) disruption and brain water content. We further demonstrated that ATX exerted anti-neuroinflammatory effects by inhibiting microglia activation and production of pro-inflammatory mediators (TNF-α and IL-1β). ATX administration attenuated ICH-induced oxidative stress by reducing the level of malondialdehyde (MDA) and restoring the activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD). Moreover, ATX promoted nuclear factor erythroid 2-related factor 2 (Nrf2) protein translocation from cytoplasm to nucleus and increased the expression of Nrf2-antioxidant response element (ARE) downstream factors such as heme oxygenase-1 (HO-1) and NADPH quinine oxidoreductase-1 (NQO-1) after ICH. Taken together, these data provided the first evidence that astaxanthin exerted neuroprotective effects in ICH mice, which suggests the Nrf2-ARE pathway was significantly correlated with the neuroprotective effects of ATX.