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

Authors

Nan Zhang, School of Pharmacy, Liaoning University of Traditional Chinese Medicine
Qingping Wen, First Affiliated Hospital, Dalian Medical University
Lu Ren, Liaoning University of Traditional Chinese Medicine
Wenbo Liang, Medical College of Dalian University
Yang Xia, College of Engineering, University of California Berkeley
Xiaodan Zhang, School of Pharmacy, Liaoning University of Traditional Chinese Medicine
Dan Zhao, School of Pharmacy, Liaoning University of Traditional Chinese Medicine
Dong Sun, School of Pharmacy, Liaoning University of Traditional Chinese Medicine
Yv Hu, School of Pharmacy, Liaoning University of Traditional Chinese Medicine
Haiguang Hao, School of Pharmacy, Liaoning University of Traditional Chinese Medicine
Yaping Yan, Department of Neurology, Thomas Jefferson UniversityFollow
Guangxian Zhang, Department of Neurology, Thomas Jefferson UniversityFollow
Jingxian Yang, School of Pharmacy, Liaoning University of Traditional Chinese MedicineFollow
Tingguo Kang, School of Pharmacy, Liaoning University of Traditional Chinese Medicine

Document Type

Article

Publication Date

9-10-2013

Comments

This article has been peer reviewed. It was published in: International Journal of Molecular Sciences.
Volume 14, Issue 9, 10 September 2013, Pages 18657-18669.
The published version is available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3794801/. DOI: 10.3390/ijms140918657

Copyright © 2013 by the authors; licensee MDPI, Basel, Switzerland.

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.

Recommended Citation

Zhang, Nan; Wen, Qingping; Ren, Lu; Liang, Wenbo; Xia, Yang; Zhang, Xiaodan; Zhao, Dan; Sun, Dong; Hu, Yv; Hao, Haiguang; Yan, Yaping; Zhang, Guangxian; Yang, Jingxian; and Kang, Tingguo, "Neuroprotective effect of arctigenin via upregulation of P-CREB in mouse primary neurons and human SH-SY5Y neuroblastoma cells." (2013). Department of Neurology Faculty Papers. Paper 61.
https://jdc.jefferson.edu/neurologyfp/61

PubMed ID

24025424