Abstract
ObjectiveThe purpose of this study was to evaluate the effect of astaxanthin (AST) on cognition function, inflammatory response and oxidative stress in vascular dementia (VD) mice.MethodVD mice model was established by left unilateral common carotid arteries occlusion (LUCCAO). Following LUCCAO, AST was intragastrically administered for 30 days. Object recognition test and morris water maze test were used to evaluate cognitive function. Hematoxylin and eosin staining was performed to observe the hippocampal neuron structure. Enzyme-linked immunosorbent assay kit and bicinchoninic acid kit were respectively adopted to measure IL-1β and IL-4 protein expression and superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in hippocampus and prefrontal cortex.ResultsAST improved the discrimination ability of VD mice. The escape latency and path length of VD mice treated with AST were dramatically reduced. Besides, AST 200 mg/kg enhanced crossing platform time and the number of times crossing the platform quadrant, and alleviated the morphological impairment in VD mice. Moreover, we found that AST inhibited IL-1β expression and MDA content, whereas promoted IL-4 expression and SOD activity in a dose-dependent manner.ConclusionAST could improve cognitive impairment and hippocampal neurons in VD mice, which may be related to suppression of inflammatory response and oxidative stress.
Highlights
Vascular dementia (VD) refers to acquired intelligence disorder syndrome, which is caused by the longterm exposure to various risk factors of cerebral vascular diseases such as cerebral ischemia and hypoxic damage [1]
AST could improve cognitive impairment and hippocampal neurons in VD mice, which may be related to suppression of inflammatory response and oxidative stress
This study was designed to analyze the effect of AST on VD mice model induced by left unilateral common carotid artery occlusion (UCCAO) (LUCCAO), and to explore whether its effect was involved in inflammatory response and oxidative stress
Summary
AST improved the discrimination ability of VD mice. The escape latency and path length of VD mice treated with AST were dramatically reduced. AST 200 mg/kg enhanced crossing platform time and the number of times crossing the platform quadrant, and alleviated the morphological impairment in VD mice. We found that AST inhibited IL-1β expression and MDA content, whereas promoted IL-4 expression and SOD activity in a dosedependent manner
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