Neuroprotective effect of astaxanthin-s-allyl cysteine diester (AST-SAC) against high glucose (HG)-induced oxidative stress in in vitro and cognitive decline under diabetes conditions in in vivo has been explored. Pretreatment of AST-SAC (5, 10 and 15 μM) dose-dependently preserved the neuronal cells (SH-SY5Y) viability against HG toxicity through i) decreasing oxidative stress (decreasing reactive oxygen species generation and increasing endogenous antioxidants level); ii) protecting mitochondrial function [oxidative phosphorylation (OXPHOS) complexes activity and mitochondrial membrane potential (MMP)]; and iii) decreasing p53 level thereby subsequently decreasing the level of apoptotic marker proteins. Male Spraque-Dawley rats were orally administered AST-SAC (1 mg/kg/day) for 45 days in streptozotocin-induced diabetes mellitus (DM) rats. AST-SAC administration prevented the loss of spatial memory in DM rats as determined using the novel object location test. AST-SAC administration alleviated the DM-induced injury in brain such as increased cholinesterases activity, elevated oxidative stress and mitochondrial dysfunction. Altogether, the results from the present study demonstrated that AST-SAC averted the neuronal apoptosis and preserved the cognitive function against HG toxicity under DM conditions.

虾青素-s-烯丙基半胱氨酸二酯 (AST-SAC) 对体外高糖 (HG) 诱导的氧化应激和体内糖尿病条件下认知能力下降的神经保护作用已被探索。AST-SAC（5、10 和 15 μM）的预处理剂量依赖性地保留了神经元细胞（SH-SY5Y）对抗 HG 毒性的活力，方法是 i）减少氧化应激（减少活性氧的产生和增加内源性抗氧化剂水平）；ii) 保护线粒体功能[氧化磷酸化 (OXPHOS) 复合物活性和线粒体膜电位 (MMP)]；iii) 降低 p53 水平，从而随后降低凋亡标记蛋白的水平。雄性 Spraque-Dawley 大鼠在链脲佐菌素诱导的糖尿病 (DM) 大鼠中口服 AST-SAC (1 mg/kg/天) 45 天。AST-SAC 给药可防止 DM 大鼠的空间记忆丧失，如使用新物体定位测试确定的那样。AST-SAC 给药减轻了 DM 引起的脑损伤，例如胆碱酯酶活性增加、氧化应激升高和线粒体功能障碍。总而言之，本研究的结果表明，AST-SAC 在 DM 条件下避免了神经元凋亡并保留了针对 HG 毒性的认知功能。