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

  • Yang, Ji Seon (Department of Physiology, College of Medicine, Catholic Neuroscience Institute, The Catholic University of Korea) ;
  • Jeon, Sujeong (Department of Physiology, College of Medicine, Catholic Neuroscience Institute, The Catholic University of Korea) ;
  • Yoon, Kee Dong (College of Pharmacy, The Catholic University of Korea) ;
  • Yoon, Shin Hee (Department of Physiology, College of Medicine, Catholic Neuroscience Institute, The Catholic University of Korea)
  • Received : 2018.07.05
  • Accepted : 2018.09.27
  • Published : 2018.11.01

Abstract

Increasing evidence implicates changes in $[Ca^{2+}]_i$ and oxidative stress as causative factors in amyloid beta ($A{\beta}$)-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 $Ca^{2+}$ and $Zn^{2+}$ signaling. The present study aimed to determine whether C3G exerts a protective effect against $A{\beta}_{25-35}$-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 $Ca^{2+}$, $Zn^{2+}$, MMP and ROS. Treatment with $A{\beta}_{25-35}$ ($20{\mu}M$) 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 $A{\beta}_{25-35}$-induced $[Zn^{2+}]_i$ increases as well as $[Ca^{2+}]_i$ increases in the cultured rat hippocampal neurons. C3G also significantly inhibited $A{\beta}_{25-35}$-induced mitochondrial depolarization. C3G also blocked the $A{\beta}_{25-35}$-induced formation of ROS. In addition, C3G significantly inhibited the $A{\beta}_{25-35}$-induced activation of caspase-3. These results suggest that cyanidin-3-glucoside protects against amyloid ${\beta}$-induced neuronal cell death by reducing multiple apoptotic signals.

Keywords

References

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