中国神经再生研究(英文版) ›› 2017, Vol. 12 ›› Issue (6): 953-958.doi: 10.4103/1673-5374.208590

• 原著:脊髓损伤修复保护与再生 • 上一篇    下一篇

灵芝多糖对体外氧化应激引起的神经元凋亡具有保护作用

  

  • 收稿日期:2017-04-30 出版日期:2017-06-15 发布日期:2017-06-15

Neuroprotective effects of ganoderma lucidum polysaccharides against oxidative stress-induced neuronal apoptosis

Xin-zhi Sun1, Ying Liao2, 3, Wei Li2, Li-mei Guo3   

  1. 1Department of Orthopedics, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China; 2 Department of Public Security Technology, Railway Police College, Zhengzhou, Henan Province, China; 3 Department of Pathology, Peking University Health Science Center, Beijing, China
  • Received:2017-04-30 Online:2017-06-15 Published:2017-06-15
  • Contact: Li-mei Guo, M.D.,guolimei16@sohu.com.

摘要:

研究证灵芝提取物灵芝多糖对缺血再灌注模型神经元凋亡有保护作用,但机制尚不明确,实验拟阐明灵芝多糖对氧化应激引起神经元凋亡作用的机制。采用H2O2诱导建立大鼠小脑颗粒神经元凋亡体外模型,以灵芝多糖添加至培养基后发现,灵芝多糖可显著拮抗H2O2引起小脑颗粒神经元的凋亡,降低细胞中促凋亡蛋白Caspase-3Bax和Bim的表达,上调抑凋亡蛋白Bcl-2的表达。结果说明灵芝多糖调节凋亡相关蛋白的表达,从而抑制了氧化应激引起的神经元凋亡,发挥了有显著的神经元保护效应。

ORCID:0000-0002-4472-2705(Li-mei Guo)

关键词: 神经再生, 脑损伤, 灵芝, 多糖, 双氧水, 氧化应激, 凋亡, 小脑颗粒神经元, Bim, Bax, Bcl-2, 细胞色素C, Caspase-3

Abstract:

Ganoderma lucidum polysaccharides have protective effects against apoptosis in neurons exposed to ischemia/reperfusion injury, but the mechanisms are unclear. The goal of this study was to investigate the underlying mechanisms of the effects of ganoderma lucidum polysaccharides against oxidative stress-induced neuronal apoptosis. Hydrogen peroxide (H2O2) was used to induce apoptosis in cultured cerebellar granule cells. In these cells, ganoderma lucidum polysaccharides remarkably suppressed H2O2-induced apoptosis, decreased expression of caspase-3, Bax and Bim and increased that of Bcl-2. These findings suggested that ganoderma lucidum polysaccharides regulate expression of apoptosis-associated proteins, inhibit oxidative stress-induced neuronal apoptosis and, therefore, have significant neuroprotective effects.

Key words: nerve regeneration, brain injury, H2O2, cerebellar granule cells, Bim, Bax, Bcl-2, cytochrome C, caspase-3, neural regeneration