Protective effect of astaxanthin on acute cerebral infarction in rats

The aim of the study was to investigate the effect of astaxanthin and its possible mechanisms on acute cerebral infarction (ACI) in rat model. Male Sprague Dawley rats were randomly divided into sham group, model group, and astaxanthin-treated groups (20, 40, and 80 mg/kg). Neurological examination, the ratio of cerebral edema, and histopathology changes were assessed. Moreover, some oxidative stress markers were obtained for biochemical analysis, and the expression of neurotrophic factors gene was detected by real-time polymerase chain reaction (RT-PCR) method. The results showed that treatment with astaxanthin notably reduced neurological deficit scores and the ratio of cerebral edema compared with the model group. Meanwhile, astaxanthin increased the activity of catalase, superoxide dismutase, and glutathioneperoxidase as well as decreased the content of malondialdehyde in brain tissue. RT-PCR results showed that the expression of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) mRNA were increased with astaxanthin treatment. The results indicated that astaxanthin could ameliorate ACI followed by suppressing oxidative stress and upregulating the expression of BDNF and NGF mRNA.

本研究旨在探讨虾青素对大鼠急性脑梗死（ACI）的影响及其可能的作用机制。将雄性Sprague Dawley大鼠随机分为假手术组、模型组和虾青素治疗组（20、40和80 mg/kg）。对神经学检查、脑水肿比率以及组织病理学变化进行评估。此外，获取一些氧化应激标志物进行生化分析，并通过实时聚合酶链反应（RT - PCR）方法检测神经营养因子基因的表达。结果显示，与模型组相比，虾青素治疗显著降低了神经功能缺损评分和脑水肿比率。同时，虾青素提高了脑组织中过氧化氢酶、超氧化物歧化酶和谷胱甘肽过氧化物酶的活性，并降低了丙二醛的含量。RT - PCR结果表明，随着虾青素治疗，脑源性神经营养因子（BDNF）和神经生长因子（NGF）mRNA的表达增加。结果表明，虾青素可通过抑制氧化应激以及上调BDNF和NGF mRNA的表达来改善ACI。