Liu Ning, Zeng Liang, Zhang Yi-Ming, Pan Wang, Lai Hong
1Department of Human Anatomy, College of Basic Medicine, China Medical University, Shenyang; Department of Radiology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning Province, China.
Department of Human Anatomy, College of Basic Medicine, Shenyang Medical College, Shenyang, Liaoning Province, China.
Neural Regen Res. 2021 Jun;16(6):1062-1067. doi: 10.4103/1673-5374.300460.
Oxidative stress is currently considered to be the main cause of brain aging. Astaxanthin can improve oxidative stress under multiple pathological conditions. It is therefore hypothesized that astaxanthin might have therapeutic effects on brain aging. To validate this hypothesis and investigate the underlying mechanisms, a mouse model of brain aging was established by injecting amyloid beta (Aβ)25-35 (5 μM, 3 μL/injection, six injections given every other day) into the right lateral ventricle. After 3 days of Aβ injections, the mouse models were intragastrically administered astaxanthin (0.1 mL/d, 10 mg/kg) for 30 successive days. Astaxanthin greatly reduced the latency to find the platform in the Morris water maze, increased the number of crossings of the target platform, and increased the expression of brain-derived neurotrophic factor, synaptophysin, sirtuin 1, and peroxisome proliferator-activated receptor-γ coactivator 1α. Intraperitoneal injection of the sirtuin 1 inhibitor nicotinamide (500 μM/d) for 7 successive days after astaxanthin intervention inhibited these phenomena. These findings suggest that astaxanthin can regulate the expression of synaptic proteins in mouse hippocampus through the sirtuin 1/peroxisome proliferator-activated receptor-γ coactivator 1α signaling pathway, which leads to improvements in the learning, cognitive, and memory abilities of mice. The study was approved by the Animal Ethics Committee, China Medical University, China (approval No. CMU2019294) on January 15, 2019.
氧化应激目前被认为是大脑衰老的主要原因。虾青素可以在多种病理条件下改善氧化应激。因此，推测虾青素可能对大脑衰老具有治疗作用。为了验证这一假设并探究其潜在机制，通过向右侧脑室注射淀粉样蛋白β（Aβ）25-35（5 μM，3 μL/注射，每隔一天注射六次）建立大脑衰老小鼠模型。在注射Aβ 3天后，对小鼠模型连续30天灌胃给予虾青素（0.1 mL/天，10 mg/kg）。虾青素显著缩短了在莫里斯水迷宫中找到平台的潜伏期，增加了穿越目标平台的次数，并增加了脑源性神经营养因子、突触素、沉默调节蛋白1和过氧化物酶体增殖物激活受体γ共激活因子1α的表达。在虾青素干预后连续7天腹腔注射沉默调节蛋白1抑制剂烟酰胺（500 μM/天）可抑制这些现象。这些发现表明，虾青素可通过沉默调节蛋白1/过氧化物酶体增殖物激活受体γ共激活因子1α信号通路调节小鼠海马体中突触蛋白的表达，从而改善小鼠的学习、认知和记忆能力。该研究于2019年1月15日获得中国医科大学动物伦理委员会批准（批准号：CMU2019294）。
