β-asarone prevents Aβ25-35-induced inflammatory responses and autophagy in SH-SY5Y cells: down expression Beclin-1, LC3B and up expression Bcl-2.

Alzheimer's disease (AD) is a chronic progressive neurodegenerative disorder. Inflammatory responses and autophagy have been implicated in the amyloid-β (Aβ) aggregation in Alzheimer's disease. Although major evidence indicates that macro autophagy is involved in the pathogenesis of AD, its exact role is still unclear. β-asarone, a major component of Acorus tatarinowii Schott, has various neuroprotective effects. However, little is known about the protection of β-asarone against inflammation response and autophagy. In the present study, we investigated the neuroprotective effects of β-asarone on Aβ25-35 induced inflammatory responses and autophagy, and the possible mechanism. Our results showed that β-asarone attenuated inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 production. Meanwhile, β-asarone could significantly reduce Beclin-1, LC3B and increase anti-apoptotic protein Bcl-2 level. These results showed that β-asarone protected cells from Aβ25-35 induced inflammation and attenuated autophagy via Bcl-2/Beclin-1 pathway. Our findings suggested that β-asarone might be a potential preventive drug for AD.