LAUSR

BACKGROUND Semaglutide, a glucagon-like peptide-1 (GLP-1) analogue with an extended half-life of approximately 1 week has being come into clinic trial to treat parkingson's disease but little is known about its effect to prevent against Alzheimer's disease (AD). The goal of the present study was to explore the potential mechanisms of semaglutide to protect against AD. METHODS We treated SH-SY5Y cell line with Aβ25-35 as an AD model. Further, SH-SY5Y cells damaged by Aβ25-35 were treated by semaglutide. Autophagy-related proteins and apoptosis-related proteins were measured to explore molecular mechanisms for semaglutide to protect against Aβ25-35. RESULTS Semaglutide enhanced autophagy by increasing the expression of LC3II, Atg7, Beclin-1 and P62 which were inhibited by Aβ25-35. Further we showed that semaglutide inhibited apoptosis by inhibiting the expression of Bax induced by Aβ25-35 and increasing the expression of Bcl2 inhibited by Aβ25-35. CONCLUSION Our results provide a clue for the hypothesis that autophagy enhancement and apoptosis inhibition may be involved in the effect of semaglutide to protect against Aβ 25-35.