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作者

Wang Yi Fu Xiaoting Li Dawei Wang Kun Wang Xinzhi Li Yuan Sun Baoliang Yang Xiaoyi Zheng Zuncheng Cho Nam Chun

作者单位

Department of Ophthalmology，Chonbuk National University，Jeonju-si，Jeollabuk-do，Republic of Korea；Department of Ophthalmology，Chonbuk National University，Jeonju-si，Jeollabuk-do，Republic of Korea；Taishan Medical University，Key Lab of Cerebral，Taian，Shandong China；Taishan Medical University，Key Lab of Cerebral，Taian，Shandong China；Taishan Medical University，Key Lab of Cerebral，Taian，Shandong China；Taishan Medical University，Key Lab of Cerebral，Taian，Shandong China；Taishan Medical University，Key Lab of Cerebral，Taian，Shandong China；Taishan Medical University，Key Lab of Cerebral，Taian，Shandong China；Taishan Medical University，Key Lab of Cerebral，Taian，Shandong China；Department of Rehabilitation，Taian Central Hospital，Shandong China.

刊名

中国神经再生研究

年份

2016

卷号

第11卷

期号

第5期

页码

795-800

关键词

nerve regeneration cyanidin amyloid-beta oxidative damage reactive oxide species apoptosis neural regeneration

摘要

Amyloid beta -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 Abeta-induced neurotoxicity in PC12 cells, and explored the underlying mechanisms. Cyanidin pretreatment significantly attenuated Abeta-induced cell mortality and morphological chang...更多

Amyloid beta -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 Abeta-induced neurotoxicity in PC12 cells, and explored the underlying mechanisms. Cyanidin pretreatment significantly attenuated Abeta-induced cell mortality and morphological changes in PC12 cells. Mechanistically, cyanidin effectively blocked apoptosis induced by Abeta, by restoring the mitochondrial membrane potential via upregulation of Bcl-2 protein expression. Moreover, cyanidin markedly protected PC12 cells from Abeta-induced DNA damage by blocking reactive oxide species and superoxide accumulation. These results provide evidence that cyanidin suppresses Abeta-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 Abeta neurotoxicity.收起

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