Li Xiaoying, Zhang Ping, Li Hongrui, Yu Huiyan, Xi Yuandi
Department of Geriatrics, Beijing Jishuitan Hospital, Beijing, China.
Department of Nutrition and Food Hygiene, School of Public Health, Capital Medical University, Beijing, China.
Front Behav Neurosci. 2022 Jun 23;16:912896. doi: 10.3389/fnbeh.2022.912896. eCollection 2022.
Zeaxanthin (ZEA) as one of the biologically active phytochemicals presents a neuroprotective effect. Since ZEA may play its anti-oxidative role in neurodegenerative diseases including Alzheimer's disease (AD), we hypothesized cognitive defects could be prevented or deferred by ZEA pre-treatment.
All the rats were randomly divided into four groups (control, Aβ1-42, ZEA, and ZEA + Aβ groups). Learning and memory ability of rats, cerebrovascular ultrastructure changes, the redox state, endothelin-1 (ET-1) level, and amyloid-β peptide (Aβ) level in plasma and the Aβ transport receptors which are advanced glycation end products (RAGEs) and LDL receptor-related protein-1 (LRP-1) and interleukin-1β (IL-1β) expressions in the cerebrovascular tissue were measured in the present study.
The escape latency and frequency of spanning the position of platform showed significant differences between the Aβ group and ZEA treatment groups. ZEA could prevent the ultrastructure changes of cerebrovascular tissue. In addition, ZEA also showed the protective effects on regulating redox state, restraining ET-1 levels, and maintaining Aβ homeostasis in plasma and cerebrovascular. Moreover, the disordered expressions of RAGE and LRP-1 and IL-1β induced by Aβ1-42 could be prevented by the pre-treatment of ZEA.
ZEA pre-treatment could prevent learning and memory impairment of rats induced by Aβ1-42. This neuroprotective effect might be attributable to the anti-oxidative and anti-inflammatory effects of ZEA on maintaining the redox state and reducing the Aβ level through regulating the Aβ transport receptors and inflammatory cytokine of the cerebrovascular tissue.
玉米黄质（ZEA）作为一种生物活性植物化学物质具有神经保护作用。由于ZEA可能在包括阿尔茨海默病（AD）在内的神经退行性疾病中发挥抗氧化作用，我们推测ZEA预处理可以预防或延缓认知缺陷。
将所有大鼠随机分为四组（对照组、Aβ1-42组、ZEA组和ZEA+Aβ组）。本研究测量了大鼠的学习和记忆能力、脑血管超微结构变化、氧化还原状态、血浆中内皮素-1（ET-1）水平和淀粉样β肽（Aβ）水平，以及脑血管组织中作为晚期糖基化终产物（RAGEs）的Aβ转运受体、低密度脂蛋白受体相关蛋白-1（LRP-1）和白细胞介素-1β（IL-1β）的表达。
Aβ组与ZEA治疗组之间的逃避潜伏期和跨越平台位置的频率存在显著差异。ZEA可以预防脑血管组织的超微结构变化。此外，ZEA在调节氧化还原状态、抑制ET-1水平以及维持血浆和脑血管中的Aβ稳态方面也显示出保护作用。而且，ZEA预处理可以预防Aβ1-42诱导的RAGE、LRP-1和IL-1β的表达紊乱。
ZEA预处理可以预防Aβ1-42诱导的大鼠学习和记忆损伤。这种神经保护作用可能归因于ZEA通过调节脑血管组织的Aβ转运受体和炎性细胞因子来维持氧化还原状态和降低Aβ水平的抗氧化和抗炎作用。
