中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (5): 795-800.doi: 10.4103/1673-5374.182707

• 原著:退行性病与再生 • 上一篇    下一篇

花青素抑制PC12细胞活性氧介导DNA损害减轻淀粉样β蛋白的神经毒性

  

  • 收稿日期:2015-12-22 出版日期:2016-05-20 发布日期:2016-05-20
  • 基金资助:

    山东省自然科学基金(ZR2014HM046)

Cyanidin suppresses amyloid beta-induced neurotoxicity by inhibiting reactive oxygen species-mediated DNA damage and apoptosis in PC12 cells

Yi Wang1, 2, #, Xiao-ting Fu2, #, Da-wei Li2, Kun Wang2, Xin-zhi Wang2, Yuan Li2, Bao-liang Sun2, Xiao-yi Yang2, Zun-cheng Zheng3, *, Nam Chun Cho1, *   

  1. "1 Department of Ophthalmology, Chonbuk National University Medical College, Jeonju-si, Jeollabuk-do, Republic of Korea 2 Key Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, Shandong Province, China 3 Department of Rehabilitation, Taian Central Hospital, Taian, Shandong Province, China"
  • Received:2015-12-22 Online:2016-05-20 Published:2016-05-20
  • Contact: Zun-cheng Zheng, M.D or Nam Chun Cho, Ph.D., zhengzc1965@126.com or cnauo@jbnu.ac.kr.
  • Supported by:

    The study was supported by the Natural Science Foundation of Shandong Province of China, No. ZR2014HM046 (to ZCZ).

摘要:

淀粉样β蛋白诱导的氧化应激是阿尔茨海默病的主要病理特点。天然黄酮化合物花青素可对抗氧化损伤介导的神经退行性病变,但机制尚不明了。由此,实验通过研究花青素对抗淀粉样β蛋白诱导的PC12细胞神经毒性,探讨相关神经保护作用机制。结果显示,花青素预处理可明显减轻淀粉样β蛋白诱导PC12细胞死亡和形态改变。花青素预处理通过影响Bcl-2家族表达,恢复线粒体膜电位,从而抑制淀粉样β蛋白诱导的PC12细胞凋亡。花青素预处理还可通过抑制过氧化反应,减轻淀粉样β蛋白诱导的PC12细胞DNA损害。说明花青素通过抑制氧自由基介导的氧化损害、抑制线粒体介导的细胞凋亡,可减轻淀粉样β蛋白诱导的细胞毒性。

orcid: 0000-0002-4021-4084(Zun-cheng Zheng)

关键词: 神经再生, 花青素, 淀粉样β蛋白, 氧化损害, 活性氧, 凋亡

Abstract:

"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."

Key words: nerve regeneration, cyanidin, amyloid-beta, oxidative damage, reactive oxide species, apoptosis, neural regeneration