Cyanidin-3-glucoside inhibits amyloid β_25-35-induced neuronal cell death in cultured rat hippocampal neurons

다국어 초록 (Multilingual Abstract)

Increasing evidence implicates changes in [Ca₂₊]_i and oxidative stress as causative factors in amyloid beta (Aβ)-induced neuronal cell death. Cyanidin-3-glucoside (C3G), a component of anthocyanin, has been reported to protect against glutamate-induced neuronal cell death by inhibiting Ca₂₊ and Zn₂₊ signaling. The present study aimed to determine whether C3G exerts a protective effect against Aβ_25-35-induced neuronal cell death in cultured rat hippocampal neurons from embryonic day 17 fetal Sprague-Dawley rats using MTT assay for cell survival, and caspase-3 assay and digital imaging methods for Ca₂₊, Zn₂₊, MMP and ROS. Treatment with Aβ_25-35 (20M) for 48 h induced neuronal cell death in cultured rat pure hippocampal neurons. Treatment with C3G for 48 h significantly increased cell survival. Pretreatment with C3G for 30 min significantly inhibited Aβ_25-35-induced [Zn₂₊]_i increases as well as [Ca₂₊]_i increases in the cultured rat hippocampal neurons. C3G also significantly inhibited Aβ_25-35-induced mitochondrial depolarization. C3G also blocked the Aβ_25-35-induced formation of ROS. In addition, C3G significantly inhibited the Aβ_25-35-induced activation of caspase-3. These results suggest that cyanidin-3-glucoside protects against amyloid -induced neuronal cell death by reducing multiple apoptotic signals.

목차 (Table of Contents)

• INTRODUCTION
• METHODS
• RESULTS
• DISCUSSION
• ACKNOWLEDGEMENTS
• CONFLICTS OF INTEREST