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KMID : 0811720180220060689
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Korean Journal of Physiology & Pharmacology
2018 Volume.22 No. 6 p.689 ~ p.696
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Cyanidin-3-glucoside inhibits amyloid β25?35-induced neuronal cell death in cultured rat hippocampal neurons
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Yang Ji-Seon
Jeon Su-Jeong
Yoon Kee-Dong
Yoon Shin-Hee
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Abstract
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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.
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KEYWORD
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Amyloid β25?35, Cyanidin-3-glucoside, Hippocampal neurons, Mitochondrial membrane potential, Neuroprotection
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