Neuroprotective Effect of Arctigenin via Upregulation of P-CREB in Mouse Primary Neurons and Human SH-SY5Y Neuroblastoma Cells

International Journal of Molecular Sciences

Nan Zhang³  Qingping Wen¹  Lu Ren⁵  Wenbo Liang⁶  Yang Xia⁴  Xiaodan Zhang³  Dan Zhao³  Dong Sun³  Yv Hu³  Haiguang Hao³  Yaping Yan²  Guangxian Zhang²  Jingxian Yang³ 

[1] First Affiliated Hospital, Dalian Medical University, Dalian 116011, Liaoning, China; E-Mail:;Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA; E-Mails:;School of Pharmacy, Liaoning University of Traditional Chinese Medicine, Dalian 116600, Liaoning, China; E-Mails:;College of Engineering, University of California Berkeley, Berkeley, CA 94720, USA; E-Mail:;Liaoning University of Traditional Chinese Medicine, Shenyang 110847, Liaoning, China; E-Mail:;Medical College of Dalian University, Dalian 116600, Liaoning, China; E-Mail:

关键词: arctigenin;    neuroprotection;    beta amyloid (Aβ);    p-CREB;   

DOI  :  10.3390/ijms140918657

来源: mdpi

【 摘 要 】

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.

【 授权许可】

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