The Protective Effects of Zeaxanthin on Amyloid-β Peptide 1-42-Induced Impairment of Learning and Memory Ability in Rats

Background and Objectives: 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. Methods and Study Design: All the rats were randomly divided into four groups (control, A beta 1-42, ZEA, and ZEA + A beta groups). Learning and memory ability of rats, cerebrovascular ultrastructure changes, the redox state, endothelin-1 (ET-1) level, and amyloid-beta peptide (A beta) level in plasma and the A beta transport receptors which are advanced glycation end products (RAGEs) and LDL receptor-related protein-1 (LRP-1) and interleukin-1 beta (IL-1 beta) expressions in the cerebrovascular tissue were measured in the present study. Results: The escape latency and frequency of spanning the position of platform showed significant differences between the A beta 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 A beta homeostasis in plasma and cerebrovascular. Moreover, the disordered expressions of RAGE and LRP-1 and IL-1 beta induced by A beta 1-42 could be prevented by the pre-treatment of ZEA. Conclusion: ZEA pre-treatment could prevent learning and memory impairment of rats induced by A beta 1-42. This neuroprotective effect might be attributable to the anti-oxidative and anti-inflammatory effects of ZEA on maintaining the redox state and reducing the A beta level through regulating the A beta transport receptors and inflammatory cytokine of the cerebrovascular tissue.