Cyanidin-3-glucoside inhibits amyloid β₂₅₋₃₅-induced neuronal cell death in cultured rat hippocampal neurons.
10.4196/kjpp.2018.22.6.689
- Author:
Ji Seon YANG
1
;
Sujeong JEON
;
Kee Dong YOON
;
Shin Hee YOON
Author Information
1. Department of Physiology, College of Medicine, Catholic Neuroscience Institute, The Catholic University of Korea, Seoul 06591, Korea. s-hyoon@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Amyloid β₂₅₋₃₅;
Cyanidin-3-glucoside;
Hippocampal neurons;
Mitochondrial membrane potential;
Neuroprotection
- MeSH:
Amyloid*;
Animals;
Anthocyanins;
Caspase 3;
Cell Death*;
Cell Survival;
Membrane Potential, Mitochondrial;
Neurons*;
Neuroprotection;
Oxidative Stress;
Rats*;
Rats, Sprague-Dawley
- From:The Korean Journal of Physiology and Pharmacology
2018;22(6):689-696
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
