BDMC protects AD in vitro via AMPK and SIRT1.

Background - Alzheimer's disease (AD) is a common neurodegenerative disorder without any satisfactory therapeutic approaches. AD is mainly characterized by the deposition of beta-amyloid protein (A beta) and extensive neuronal cell death. Curcumin, with anti-oxidative stress (OS) and cell apoptosis properties, plays essential roles in AD. However, whether bisdemethoxycurcumin (BDMC), a derivative of curcumin, can exert a neuroprotective effect in AD remains to be elucidated. Methods - In this study, SK-N-SH cells were used to establish an in vitro model to investigate the effects of BDMC on the A beta 1-42-induced neurotoxicity. SK-N-SH cells were pretreated with BDMC and with or without compound C and EX527 for 30 min after co-incubation with rotenone for 24 h. Subsequently, western blotting, cell viability assay and SOD and GSH activity measurement were performed. Results - BDMC increased the cell survival, anti-OS ability, AMPK phosphorylation levels and SIRT1 in SK-NSH cells treated with A beta 1-42. However, after treatment with compound C, an AMPK inhibitor, and EX527, an SIRT1inhibitor, the neuroprotective roles of BDMC on SKN-SH cells treated with A beta 1-42 were inhibited. Conclusion - These results suggest that BDMC exerts a neuroprotective role on SK-N-SH cells in vitro via AMPK/SIRT1 signaling, laying the foundation for the application of BDMC in the treatment of neurodegenerative diseases related to AMPK/SIRT1 signaling.