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KCI등재 학술저널

Cyanidin-3-glucoside inhibits amyloid β<sub>25-35</sub>-induced neuronal cell death in cultured rat hippocampal neurons

Cyanidin-3-glucoside inhibits amyloid β<sub>25-35</sub>-induced neuronal cell death in cultured rat hippocampal neurons

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Increasing evidence implicates changes in [Ca<sub>2+</sub>]<sub>i</sub> 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 Ca<sub>2+</sub> and Zn<sub>2+</sub> signaling. The present study aimed to determine whether C3G exerts a protective effect against Aβ<sub>25-35</sub>-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 Ca<sub>2+</sub>, Zn<sub>2+</sub>, MMP and ROS. Treatment with Aβ<sub>25-35</sub> (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<sub>25-35</sub>-induced [Zn<sub>2+</sub>]<sub>i</sub> increases as well as [Ca<sub>2+</sub>]<sub>i</sub> increases in the cultured rat hippocampal neurons. C3G also significantly inhibited Aβ<sub>25-35</sub>-induced mitochondrial depolarization. C3G also blocked the Aβ<sub>25-35</sub>-induced formation of ROS. In addition, C3G significantly inhibited the Aβ<sub>25-35</sub>-induced activation of caspase-3. These results suggest that cyanidin-3-glucoside protects against amyloid -induced neuronal cell death by reducing multiple apoptotic signals.

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CONFLICTS OF INTEREST

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