Nacre extract from pearl oyster attenuates amyloid beta-induced memory impairment.

Abstract

Shells are composed of two types of calcium carbonate polymorphs-the prismatic layer and the nacreous layer. Pearls, composed of the nacreous layer, have been used in Chinese medicine since ancient times. We have previously shown that extracts from the nacreous layer improves scopolamine-induced memory impairment. However, whether pearl ameliorates cognitive disorders induced by amyloid-β 1-40 (Aβ1-40) has not been elucidated. In this study, we investigated whether nacre extract improves memory impairment induced by intracerebroventricular injection of Aβ1-40. Administration of nacre extract led to recovery from Aβ1-40-induced impairments in object recognition, short-term memory, and spatial memory. Nacre extract reversed the increase in lipid peroxidation caused by Aβ1-40 in the cerebral cortex by increasing the expression of catalase and superoxide dismutase. In addition, nacre extract recovered the expression and phosphorylation of cyclic AMP response element-binding protein (CREB), which decreased with Aβ1-40 treatment, and increased the expression of brain-derived neurotrophic factor and neuropeptide Y, which are regulated by CREB. Nacre extract also suppressed acetylcholine esterase activity and Aβ1-40-induced tau phosphorylation. Histochemical analysis of the hippocampus region showed that the nacre extract protected against Aβ1-40-induced neuronal loss in the hippocampus. These results suggest that nacre extract protects against Aβ1-40-induced neuronal cell death by suppressing oxidative stress and increasing the expression and phosphorylation of CREB.