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 Aβ25-35-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 Aβ25-35 (20 µM) 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 Aβ25-35-induced [Zn2+]i increases as well as [Ca2+]i increases in the cultured rat hippocampal neurons. C3G also significantly inhibited Aβ25-35-induced mitochondrial depolarization. C3G also blocked the Aβ25-35-induced formation of ROS. In addition, C3G significantly inhibited the Aβ25-35-induced activation of caspase-3. These results suggest that cyanidin-3-glucoside protects against amyloid β-induced neuronal cell death by reducing multiple apoptotic signals.
Keywords: Amyloid β25–35; Cyanidin-3-glucoside; Hippocampal neurons; Mitochondrial membrane potential; Neuroprotection.