Neuroprotective effect of sinapic acid in a mouse model of amyloid β1–42 protein-induced Alzheimer's disease

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Abstract

Sinapic acid (SA) is a phenylpropanoid compound with anti-inflammatory and neuroprotective activities. The neuroprotective effects of SA in a mouse model of amyloid β (Aβ)1–42 protein-induced Alzheimer's disease (AD) were investigated. Mice received a bilateral injection of Aβ1–42 protein into the hippocampus to verify the efficacy of SA. Mice were treated with SA (10 mg/kg/day, p.o.) for 7 days beginning immediately after Aβ1–42 protein injection, and an acquisition trial of the passive avoidance task was conducted 1 h after the last administration of SA. Retention trial was conducted 24 h after the acquisition trial, and mice were sacrificed for immunohistochemistry immediately after the retention trial. SA rescued neuronal cell death in the hippocampal CA1 region and also attenuated the increase of iNOS expression, glial cell activations and nitrotyrosine expressions induced by Aβ1–42 protein. SA significantly attenuated memory impairment in the passive avoidance task. These results suggest that SA ameliorated Aβ1–42 protein-related pathology including neuronal cell death and cognitive dysfunction via its anti-oxidative and anti-inflammatory activities, and may be an efficacious treatment for AD.

Highlights

▸ Sinapic acid (SA) attenuated Aβ1–42 protein-induced memory impairment in vivo study. ▸ SA attenuated Aβ1–42 protein-induced hippocampal CA1 cell death. ▸ SA exerted anti-inflammatory and anti-oxidative properties. ▸ SA can be a potential neuroprotective agent for Alzheimer's disease therapy.

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