Open AccessCyanidin suppresses amyloid beta-induced neurotoxicity by inhibiting reactive oxygen species-mediated DNA damage and apoptosis in PC12 cells
Author(s) -
Yi Wang,
Xiaoting Fu,
Dawei Li,
Kun Wang,
Xinzhi Wang,
Yuan Li,
Bo Sun,
Xiaoyi Yang,
Zuncheng Zheng,
Nam Chun Cho
Publication year - 2016
Publication title -
neural regeneration research/neural regeneration research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.93
H-Index - 38
eISSN - 1876-7958
pISSN - 1673-5374
DOI - 10.4103/1673-5374.182707
Subject(s) - neurotoxicity , reactive oxygen species , oxidative stress , cyanidin , apoptosis , amyloid beta , dna damage , neuroprotection , chemistry , microbiology and biotechnology , mitochondrion , cytotoxicity , downregulation and upregulation , programmed cell death , pharmacology , biochemistry , biology , antioxidant , toxicity , dna , in vitro , peptide , organic chemistry , gene
Amyloid beta (Aβ)-induced oxidative stress is a major pathologic hallmark of Alzheimer's disease. Cyanidin, a natural flavonoid compound, is neuroprotective against oxidative damage-mediated degeneration. However, its molecular mechanism remains unclear. Here, we investigated the effects of cyanidin pretreatment against Aβ-induced neurotoxicity in PC12 cells, and explored the underlying mechanisms. Cyanidin pretreatment significantly attenuated Aβ-induced cell mortality and morphological changes in PC12 cells. Mechanistically, cyanidin effectively blocked apoptosis induced by Aβ, by restoring the mitochondrial membrane potential via upregulation of Bcl-2 protein expression. Moreover, cyanidin markedly protected PC12 cells from Aβ-induced DNA damage by blocking reactive oxide species and superoxide accumulation. These results provide evidence that cyanidin suppresses Aβ-induced cytotoxicity, by preventing oxidative damage mediated by reactive oxide species, which in turn inhibits mitochondrial apoptosis. Our study demonstrates the therapeutic potential of cyanidin in the prevention of oxidative stress-mediated Aβ neurotoxicity.