Gastrodin protect primary cultured rat hippocampal neurons against amyloid-beta peptide-induced neurotoxicity via ERK1/2-Nrf2 pathway
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- 作者：Xuemei Zhao ; Yu Zou ; Hao Xu ; Li Fan ; Hongyan Guo ; Xiaoming Li ; Gang Li ; Xiaojie Zhang ; Miaoxian Dong
- 关键词：AD ; Alzheimer's disease ; A¦Â ; amyloid-beta ; CAT ; catalase ; SOD ; superoxide dismutase ; Nrf2 ; nuclear factor erythroid 2-related factor 2 ; ERK1/2 ; extracellular signal-regulated kinases 1 and 2 ; HBSS ; Hank's blanced salt solution ; ELISA ; enzyme-linked immun
- 刊名：Brain Research
- 出版年：2012
- 出版时间：30 October, 2012
- 年：2012
- 卷：1482
- 期：Complete
- 页码：13-21
- 全文大小：768 K
文摘
One hallmark of Alzheimer's disease (AD) is amyloid-beta (A¦Â) deposition, which can initiate a cascade of oxidative events that may result in neuronal death. The present study aimed to investigate the protective effects of gastrodin, a phenolic compound which shows antioxidant activity, on A¦Â(1-42)-induced neurotoxicity and the underlying mechanism for this neuroprotection. Results indicate that A¦Â(1-42)-induced neuronal toxicity as measured by cell viability, which was correlated with decreased catalase (CAT) content and superoxide dismutase (SOD) activity. Pre-treatment of primary hippocampal neurons with gastrodin significantly attenuated A¦Â(1-42)-induced neurotoxicity and changes in SOD and CAT, and upregulated gene expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and extracellular signal-regulated kinases 1 and 2 (ERK1/2) phosphorylation. Pharmacological blockade of ERK1/2 abrogation this action of gastrodin. The ERK1/2 pathway may be involved in the neuroprotective effect of gastrodin against A¦Â(1-42)-induced oxidative in primary cultured rat hippocampal neurons. These findings suggest that gastrodin could be of importance for the treatment of AD and other oxidative stress-related diseases.