The neuroprotective effect of astaxanthin on newborn rat models of hypoxic-ischemic brain damage

Lin Liang-feng

doi:10.3969/j.issn.2095-4344.2015.40.016

Abstract：BACKGROUND:Several studies have demonstrated that astaxanthin has a good neuroprotective effect; however, the treatment effects of astaxanthin on newborns with hypoxic-ischemic brain damage have not been reported. OBJECTIVE: To build newborn rat models of hypoxic-ischemic brain damage, and investigate the neuroprotective effects of astaxanthin and the ways of action. METHODS: Thirty newborn Sprague-Dawley rats aged 7 days out of 98 were randomly taken as sham-operated group. The rest of rats were subjected to ligature of the left carotid artery for 2 hours and then placed in the hypoxic box containing 92% special standard gas and 8% oxygen to establish the models of hypoxic-ischemic brain damage. The rats in the sham-operated group only underwent separation of the carotid arteries, without hypoxic-ischemic treatment. Rat models of hypoxic-ischemic brain damage were randomly divided into hypoxic-ischemic brain damage and astaxanthin-treated groups, with 30 rats in each group. The rats in the astaxanthin-treated group were intraperitionaly injected with 80 mg/kg astaxanthin after hypoxic-ischemic brain damage. RESULTS AND CONLUSION:Compared with the sham-operated group, the expression levels of p-Akt, p-GSK3β and cleaved-caspase-3 protein in the parietal cortex of ischemic damage area of rats were significantly increased, whereas Bcl-2 protein expression was significantly decreased in the hypoxic-ischemic brain damage group (alP < 0.05). Compared with the hypoxic-ischemic brain damage group, astaxanthin treatment significantly reduced the expression level of apoptosis-related protein cleaved-caspase 3 protein (P < 0.05), significantly increased the expression level of Bcl-2 protein (P < 0.05), and significantly reduced the number of apoptotic cels in the hypoxic-ischemic brain area(P < 0.05). These findings suggest that astaxanthin can distinctly improve the prognosis and ways of action of hypoxic-ischemic brain damage in newborn rats which associates with up-regulation of Akt/GSK3β signaling pathways.