neuroprotective effects of astaxanthin after middle cerebral artery occlusion stroke in male rats: the ca1 hippocampal region

Introduction: ischemic stroke often results in severe neurological impairment, particularly affecting the hippocampal ca1 region, which is highly vulnerable to ischemia-reperfusion injury. astaxanthin (atx), a potent antioxidant carotenoid, exhibits neuroprotective, anti-inflammatory, and anti-apoptotic properties. this study aimed to investigate the effects of atx on functional, biochemical, and histological outcomes in a focal transient middle cerebral artery occlusion (mcao) model in rats.methods: fifty-six male wistar rats were randomly assigned to seven groups: intact, sham, stroke (mcao), solvent (0.1% dimethyl sulfoxide [dmso]), and atx-treated groups (25, 50, or 100 mg/kg, intraperitoneally every 12 hours for 3 days post-mcao). neurological function (bederson score), motor coordination (rotarod), spatial learning (morris water maze [mwm]), and memory retention (passive avoidance learning [pal] using shuttle box) were assessed. cerebrospinal fluid (csf) cytokine levels (interleukin [il]-10, il-1β), cerebral edema, and hippocampal ca1 histology were analyzed.results: low (25 mg/kg) and medium (50 mg/kg) atx doses significantly improved neurological and functional performance compared with untreated mcao rats (p<0.01). these doses increased il-10, reduced il-1β levels, decreased brain water content, and preserved neuronal morphology in the ca1 region. conversely, the high dose (100 mg/kg) conferred no significant benefits. histopathology confirmed reduced neuronal damage and apoptosis at effective doses.conclusion: post-ischemic atx administration provides neuroprotection in a rat mcao model, with 25–50 mg/kg yielding optimal outcomes. the observed inverted dose-response underscores the importance of precise dosing and timing. atx represents a promising therapeutic candidate for ischemic stroke pending further translational studies.