Protective effects of astaxanthin on subarachnoid hemorrhage-induced early brain injury: Reduction of cerebral vasospasm and improvement of neuron survival and mitochondrial function

• Published in: Acta histochemica Vol. 121; no. 1; pp. 56 - 63
• Main Authors: Wang, Yanbin, Liu, Yao, Li, Yuchen, Liu, Binbing, Wu, Pei, Xu, Shancai, Shi, Huaizhang
• Format: Journal Article
• Language: English
• Published: Germany Elsevier GmbH 01.01.2019
• Subjects: Apoptosis; Astaxanthin; Cerebral vasospasm; Early brain injury; Mitochondria; Subarachnoid hemorrhage; Cerebral vasospasm; Mitochondria; Early brain injury; Subarachnoid hemorrhage; Astaxanthin; Apoptosis
• ISSN: 0065-1281; 1618-0372
• DOI: 10.1016/j.acthis.2018.10.014

•Astaxanthin exhibits a neuroprotective effect on subarachnoid hemorrhage in rats.•Astaxanthin prevents mitochondrial dysfunction in the brain.•Astaxanthin treatment attenuates subarachnoid hemorrhage-induced cerebral vasospasm.•Astaxanthin enhances the generation of nerve growth factors, including synapsin I, BDNF, GAP-43, PSD-95 and Purα. The purpose of this study was to evaluate the neuroprotective effects of astaxanthin on early brain injury (EBI) caused by subarachnoid hemorrhage (SAH) in rats and to explore possible molecular mechanisms. Experimental SAH model was introduced in adult male SD rats by injecting autologous arterial blood into the prechiasmatic cistern. Astaxanthin (75 mg/kg bodyweight) or olive oil was administered by oral gavage at 3 h after SAH. Our results showed that astaxanthin attenuated SAH-induced cerebral vasospasm and reduced neuronal apoptosis. Astaxanthin inhibited mitochondria-associated neuron apoptosis in the prefrontal cortex after SAH: increased mitochondrial membrane potential, decreased Bax/Bcl-2 ratio, inhibited cytochrome C release in cytoplasm, and suppressed caspase-3 enzyme activity. Furthermore, the cerebral expression levels of synaptic proteins (Synapsin-1, postsynaptic density-95 and growth-associated protein-43) and nerve growth and neuronal differentiation factors (brain-derived neurotropic factor and purine-rich binding protein-alpha) were reduced following SAH. Astaxanthin partly restored their expression. In conclusion, our current work demonstrates that astaxanthin attenuates SAH-induced EBI, possibly by improving neuronal survival and mitochondrial function.