Korean J Physiol Pharmacol.  2018 Nov;22(6):689-696. 10.4196/kjpp.2018.22.6.689.

Cyanidin-3-glucoside inhibits amyloid β₂₅₋₃₅-induced neuronal cell death in cultured rat hippocampal neurons

  • 1Department of Physiology, College of Medicine, Catholic Neuroscience Institute, The Catholic University of Korea, Seoul 06591, Korea. s-hyoon@catholic.ac.kr
  • 2College of Pharmacy, The Catholic University of Korea, Bucheon 14662, Korea.


Increasing evidence implicates changes in [Ca²âº]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 Ca²âº and Zn²âº 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 Ca²âº, Zn²âº, 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 [Zn²âº]i increases as well as [Ca²âº]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.


Amyloid β₂₅₋₃₅; Cyanidin-3-glucoside; Hippocampal neurons; Mitochondrial membrane potential; Neuroprotection
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