학술논문
Cyanidin-3-glucoside inhibits amyloid β25-35-induced neuronal cell death in cultured rat hippocampal neurons
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- 영문명
- Cyanidin-3-glucoside inhibits amyloid β25-35-induced neuronal cell death in cultured rat hippocampal neurons
- 발행기관
- 대한생리학회-대한약리학회
- 저자명
- Ji Seon Yang Su-jeong Jeon Kee Dong Yoon Shin Hee Yoon
- 간행물 정보
- 『The Korean Journal of Physiology & Pharmacology』제22권 제6호, 689~696쪽, 전체 8쪽
- 주제분류
- 의약학 > 의학일반
- 파일형태
- 발행일자
- 2018.11.30
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국문 초록
영문 초록
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 (20M) 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 -induced neuronal cell death by reducing multiple apoptotic signals.
목차
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
CONFLICTS OF INTEREST
키워드
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