ArticleFrontiers in neurology2026
Astaxanthin exerts neuroprotection against experimental intracerebral hemorrhage in mice: association with anti-neuroinflammation and the Nrf2-ARE pathway.
Article in Frontiers in neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.