Neuroprotective Effect of Arctigenin via Upregulation of P-CREB in Mouse Primary Neurons and Human SH-SY5Y Neuroblastoma Cells
1
School of Pharmacy, Liaoning University of Traditional Chinese Medicine, Dalian 116600, Liaoning, China
2
First Affiliated Hospital, Dalian Medical University, Dalian 116011, Liaoning, China
3
Liaoning University of Traditional Chinese Medicine, Shenyang 110847, Liaoning, China
4
Medical College of Dalian University, Dalian 116600, Liaoning, China
5
College of Engineering, University of California Berkeley, Berkeley, CA 94720, USA
6
Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA
*
Authors to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Int. J. Mol. Sci. 2013, 14(9), 18657-18669; https://doi.org/10.3390/ijms140918657
Received: 10 May 2013 / Revised: 22 July 2013 / Accepted: 23 August 2013 / Published: 10 September 2013
(This article belongs to the Special Issue Neuroprotective Strategies 2014)
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.
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Keywords:
arctigenin; neuroprotection; beta amyloid (Aβ); p-CREB
This is an open access article distributed under the Creative Commons Attribution License
MDPI and ACS Style
Zhang, N.; Wen, Q.; Ren, L.; Liang, W.; Xia, Y.; Zhang, X.; Zhao, D.; Sun, D.; Hu, Y.; Hao, H.; Yan, Y.; Zhang, G.; Yang, J.; Kang, T. Neuroprotective Effect of Arctigenin via Upregulation of P-CREB in Mouse Primary Neurons and Human SH-SY5Y Neuroblastoma Cells. Int. J. Mol. Sci. 2013, 14, 18657-18669.
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