Beta-Asarone Improves Cognitive Function by Suppressing Neuronal Apoptosis in the Beta-Amyloid Hippocampus Injection Rats

Elevated levels of beta-amyloid (A beta) in the brains being a hallmark of Alzheimer's disease (AD) have been believed to play a critical role in the cognitive dysfunction that occurs in AD. Recent evidence suggests that A beta induces neuronal apoptosis in the brain and in primary neuronal cultures. In this study, we investigated the effects of beta-asarone, the major ingredient of Acorus Tatarinowii Schott, on cognitive function and neuronal apoptosis in A beta hippocampus injection rats and its mechanism of action. The results show that the A beta (1-42) injection caused impairments in spatial reference memory in a Morris water maze task and apoptosis in hippocampus. Oral administration of beta-asarone with three different dose (12.5, 25, or 50 mg/kg) for 28 d ameliorated A beta (1-42)-induced cognitive impairment and reversed the increase of apoptosis in the hippocampus. All-induced c-Jun N-terminal kinase (JNK) results in phosphorylation, subsequent down-regulation of Bcl-2 and Bcl-w expression, and caspase-3 activation. Beta-asarone attenuate A beta (1-42)-induced neuronal apoptosis in hippocampus by reversal down-regulation of Bcl-2, Bcl-w, caspase-3 activation, and JNK phosphorylation. These results suggest that beta-asarone may be a potential candidate for development as a therapeutic agent to manage cognitive impairment associated with conditions such as Alzheimer's disease.