Department of Anatomy, College of Korean Medicine, Dongguk University, Gyeongju 38066, Korea.
Department of Food Science and Nutrition, Hallym University, Chuncheon 24252, Korea.
Mar Drugs. 2022 Apr 14;20(4):267. doi: 10.3390/md20040267.
Astaxanthin is a powerful biological antioxidant and is naturally generated in a great variety of living organisms. Some studies have demonstrated the neuroprotective effects of ATX against ischemic brain injury in experimental animals. However, it is still unknown whether astaxanthin displays neuroprotective effects against severe ischemic brain injury induced by longer (severe) transient ischemia in the forebrain. The purpose of this study was to evaluate the neuroprotective effects of astaxanthin and its antioxidant activity in the hippocampus of gerbils subjected to 15-min transient forebrain ischemia, which led to the massive loss (death) of pyramidal cells located in hippocampal cornu Ammonis 1-3 (CA1-3) subfields. Astaxanthin (100 mg/kg) was administered once daily for three days before the induction of transient ischemia. Treatment with astaxanthin significantly attenuated the ischemia-induced loss of pyramidal cells in CA1-3. In addition, treatment with astaxanthin significantly reduced ischemia-induced oxidative DNA damage and lipid peroxidation in CA1-3 pyramidal cells. Moreover, the expression of the antioxidant enzymes superoxide dismutase (SOD1 and SOD2) in CA1-3 pyramidal cells were gradually and significantly reduced after ischemia. However, in astaxanthin-treated gerbils, the expression of SOD1 and SOD2 was significantly high compared to in-vehicle-treated gerbils before and after ischemia induction. Collectively, these findings indicate that pretreatment with astaxanthin could attenuate severe ischemic brain injury induced by 15-min transient forebrain ischemia, which may be closely associated with the decrease in oxidative stress due to astaxanthin pretreatment.
虾青素是一种强大的生物抗氧化剂,天然存在于各种生物中。一些研究表明,ATX 对实验动物的缺血性脑损伤具有神经保护作用。然而,目前尚不清楚虾青素是否对前脑更长时间(严重)短暂性缺血引起的严重缺血性脑损伤具有神经保护作用。本研究旨在评估虾青素及其在 15 分钟短暂性前脑缺血导致的位于海马角 1-3(CA1-3)亚区的锥体神经元大量丧失(死亡)的沙土鼠中的抗氧化活性。虾青素(100mg/kg)在诱导短暂性缺血前每日一次连续 3 天给药。虾青素治疗显著减轻了缺血诱导的 CA1-3 锥体神经元丢失。此外,虾青素治疗显著降低了 CA1-3 锥体细胞中缺血诱导的氧化 DNA 损伤和脂质过氧化。此外,在缺血后,CA1-3 锥体细胞中的抗氧化酶超氧化物歧化酶(SOD1 和 SOD2)的表达逐渐显著降低。然而,在虾青素处理的沙土鼠中,与缺血诱导前后的载体处理的沙土鼠相比,SOD1 和 SOD2 的表达明显升高。综上所述,这些发现表明,虾青素预处理可减轻 15 分钟短暂性前脑缺血引起的严重缺血性脑损伤,这可能与虾青素预处理减少氧化应激密切相关。