Cyanidin-3-glucoside inhibits amyloid β₂₅₋₃₅-induced neuronal cell death in cultured rat hippocampal neurons
The Korean Journal of Physiology and Pharmacology
;
: 689-696, 2018.
Article
in English
| WPRIM
| ID: wpr-727856
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Cell Survival
/
Cell Death
/
Rats, Sprague-Dawley
/
Oxidative Stress
/
Caspase 3
/
Membrane Potential, Mitochondrial
/
Neuroprotection
/
Amyloid
/
Anthocyanins
/
Neurons
Limits:
Animals
Language:
English
Journal:
The Korean Journal of Physiology and Pharmacology
Year:
2018
Type:
Article
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