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Neuroprotective effect of arctigenin via upregulation of P-CREB in mouse primary neurons and human SH-SY5Y neuroblastoma cells.

Abstract
Arctigenin (Arc) has been shown to act on scopolamine-induced memory deficit mice and to provide a neuroprotective effect on cultured cortical neurons from glutamate-induced neurodegeneration through mechanisms not completely defined. Here, we investigated the neuroprotective effect of Arc on H89-induced cell damage and its potential mechanisms in mouse cortical neurons and human SH-SY5Y neuroblastoma cells. We found that Arc prevented cell viability loss induced by H89 in human SH-SY5Y cells. Moreover, Arc reduced intracellular beta amyloid (Aβ) production induced by H89 in neurons and human SH-SY5Y cells, and Arc also inhibited the presenilin 1(PS1) protein level in neurons. In addition, neural apoptosis in both types of cells, inhibition of neurite outgrowth in human SH-SY5Y cells and reduction of synaptic marker synaptophysin (SYN) expression in neurons were also observed after H89 exposure. All these effects induced by H89 were markedly reversed by Arc treatment. Arc also significantly attenuated downregulation of the phosphorylation of CREB (p-CREB) induced by H89, which may contribute to the neuroprotective effects of Arc. These results demonstrated that Arc exerted the ability to protect neurons and SH-SY5Y cells against H89-induced cell injury via upregulation of p-CREB.
AuthorsNan Zhang, Qingping Wen, Lu Ren, Wenbo Liang, Yang Xia, Xiaodan Zhang, Dan Zhao, Dong Sun, Yv Hu, Haiguang Hao, Yaping Yan, Guangxian Zhang, Jingxian Yang, Tingguo Kang
JournalInternational journal of molecular sciences (Int J Mol Sci) Vol. 14 Issue 9 Pg. 18657-69 (Sep 10 2013) ISSN: 1422-0067 [Electronic] Switzerland
PMID24025424 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Cyclic AMP Response Element-Binding Protein
  • Furans
  • Lignans
  • Neuroprotective Agents
  • arctigenin
Topics
  • Animals
  • Cell Survival (drug effects)
  • Cells, Cultured
  • Cyclic AMP Response Element-Binding Protein (metabolism)
  • Furans (pharmacology)
  • Humans
  • Lignans (pharmacology)
  • Mice
  • Neuroblastoma (metabolism)
  • Neuroprotective Agents (pharmacology)
  • Phosphorylation (drug effects)
  • Tumor Cells, Cultured

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