Lutein–Zeaxanthin Extract (XanMax ® 2002) Attenuates Oxidative Stress,Neuroinflammation,and Memory Deficits in H 2 O 2 -Exposed Neuro-2a Cells and Scopolamine-Induced Mice

Abstract

Age-related cognitive impairment is often linked to cholinergic dysfunction and increased oxidative stress. This study explored the neuroprotective potential of lutein–zeaxanthin extract (XanMax^® 2002; LZ) through both in vitro and in vivo approaches. In vitro, Neuro-2a cells exposed to hydrogen peroxide (H₂O₂) were treated with LZ (5–20 μg/mL), leading to decreased expression of apoptosis-related proteins. In vivo, memory impairment was induced by scopolamine in C57BL/6N mice, followed by oral administration of LZ (4 or 8 mg/kg) for 4 weeks. Behavioral assessments—including the Morris water maze, Y-maze, and passive avoidance tests—demonstrated significant improvements in spatial learning, working memory, and memory retention in LZ-treated groups, particularly at the higher dose. Biochemical analysis revealed increased acetylcholine levels, reduced acetylcholinesterase activity, and downregulation of oxidative stress and neuroinflammatory markers in brain tissue. Moreover, LZ supplementation upregulated genes associated with synaptic function and memory. The cognitive-enhancing effects of LZ were comparable with those of donepezil. These findings suggest that LZ may exert neuroprotective effects through antioxidant and anti-inflammatory mechanisms and are a potential dietary intervention for cognitive decline.