Salidroside Ester Prevents Apoptosis of Neurons through Suppression of Aβ-Accumulation and Down-regulation of Inflammatory Response in Alzheimer’s Disease

Abstract

The present study investigated salidroside ester, a relatively less polar derivative of
salidroside in vitro for prevention of β-amyloid induced damage in PC12 neuronal cells. Pretreatment
of PC12 cells with salidroside ester (0.12 to 32 μM) reversed β-amyloid mediated reduction in viability
in dose-dependent manner. The β-amyloid mediated reduction of PC12 cell viability was completely
prevented by salidroside ester treatment at 32 μM. The β-amyloid induced up-regulation of PGE2 expression in PC12 cells was significantly (p < 0.05) alleviated by salidroside ester pre-treatment. Salidroside ester pre-treatment also alleviated β-amyloid induced up-regulation of COX-2 expression and NO
production significantly (p <0 .05) in PC12 cells. Moreover, β-amyloid induced up-regulation of iNOS
expression in PC12 cells was significantly (p < 0.05) alleviated by salidroside ester pre-treatment. Additionally, salidroside ester pre-treatment significantly (p < 0.05) inhibited β-amyloid mediated up-regulation of NF-κB nuclear translocation in PC12 cells. Thus, salidroside ester prevents loss of PC12 cells
induced by β-amyloid stimulation through anti-inflammatory mechanism. Moreover, its pretreatment
targets β-amyloid induced increase in PGE2 and COX-2 expression and down-regulated iNOS and
NO level in PC12 cells. Therefore, salidroside ester needs to be investigated further for possible role in
prevention of neurodegenerative disorders such as Alzheimer’s disease.