β-asarone modulates Beclin-1, LC3 and p62 expression to attenuate Aβ40 and Aβ42 levels in APP/PS1 transgenic mice with Alzheimer's disease

Alzheimer's disease (AD) is a common neurodegenerative disease in the elderly population. Autophagy is a well-known regulator of neurodegenerative diseases and beta-asarone has been discovered to have certain neuropharmacological effects. Thus, the present study aimed to analyze the potential effects of beta-asarone in AD and its possible mechanism of action in relation to autophagy. The present study investigated the effects of beta-asarone on the number of senile plaques and amyloid beta(A beta)(40), A beta(42), amyloid precursor protein (APP) and Beclin-1 mRNA levels in the hippocampus of APP/presenilin-1 (PS1) transgenic mice. The possible mechanism of beta-asarone on autophagy-related proteins, including Beclin-1, light chain (LC)3A, LC3B and p62 levels, and the number of autophagosomes was also investigated. Mice were divided into a normal control group, a model group, a beta-asarone-treated group, a 3-MA-treated group and a rapamycin-treated group. Treatments were continuously administered to all mice for 30 days by intragastric administration. The mice, including those in the normal and model control groups, were given equal volumes of saline. It was demonstrated that beta-asarone treatment reduced the number of senile plaques and autophagosomes, and decreased A beta(40), A beta(42), APP and Beclin-1 expression in the hippocampus of model mice compared with untreated model mice. beta-asarone also inhibited LC3A/B expression levels, but increased p62 expression. It was deduced that the neuroprotective effects of beta-asarone in APP/PS1 transgenic mice resulted from its inhibition of autophagy. In conclusion, the data suggested that beta-asarone should be explored further as a potential therapeutic agent in AD.