Neuroprotective Effect of Arctigenin via Upregulation of P-CREB in Mouse Primary Neurons and Human SH-SY5Y Neuroblastoma Cells
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-in...
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| Format: | Article |
| Language: | English |
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MDPI AG
2013-09-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | http://www.mdpi.com/1422-0067/14/9/18657 |
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| author | Tingguo Kang Jingxian Yang Yaping Yan Guangxian Zhang Haiguang Hao Dong Sun Yv Hu Dan Zhao Yang Xia Xiaodan Zhang Wenbo Liang Lu Ren Qingping Wen Nan Zhang |
| author_facet | Tingguo Kang Jingxian Yang Yaping Yan Guangxian Zhang Haiguang Hao Dong Sun Yv Hu Dan Zhao Yang Xia Xiaodan Zhang Wenbo Liang Lu Ren Qingping Wen Nan Zhang |
| author_sort | Tingguo Kang |
| collection | DOAJ |
| description | 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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| format | Article |
| id | doaj.art-8def458484f64f158aad7d16b6d90853 |
| institution | Directory Open Access Journal |
| issn | 1422-0067 |
| language | English |
| last_indexed | 2024-04-12T09:55:37Z |
| publishDate | 2013-09-01 |
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| series | International Journal of Molecular Sciences |
| spelling | doaj.art-8def458484f64f158aad7d16b6d908532022-12-22T03:37:43ZengMDPI AGInternational Journal of Molecular Sciences1422-00672013-09-01149186571866910.3390/ijms140918657Neuroprotective Effect of Arctigenin via Upregulation of P-CREB in Mouse Primary Neurons and Human SH-SY5Y Neuroblastoma CellsTingguo KangJingxian YangYaping YanGuangxian ZhangHaiguang HaoDong SunYv HuDan ZhaoYang XiaXiaodan ZhangWenbo LiangLu RenQingping WenNan ZhangArctigenin (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.http://www.mdpi.com/1422-0067/14/9/18657arctigeninneuroprotectionbeta amyloid (Aβ)p-CREB |
| spellingShingle | Tingguo Kang Jingxian Yang Yaping Yan Guangxian Zhang Haiguang Hao Dong Sun Yv Hu Dan Zhao Yang Xia Xiaodan Zhang Wenbo Liang Lu Ren Qingping Wen Nan Zhang Neuroprotective Effect of Arctigenin via Upregulation of P-CREB in Mouse Primary Neurons and Human SH-SY5Y Neuroblastoma Cells International Journal of Molecular Sciences arctigenin neuroprotection beta amyloid (Aβ) p-CREB |
| title | Neuroprotective Effect of Arctigenin via Upregulation of P-CREB in Mouse Primary Neurons and Human SH-SY5Y Neuroblastoma Cells |
| title_full | Neuroprotective Effect of Arctigenin via Upregulation of P-CREB in Mouse Primary Neurons and Human SH-SY5Y Neuroblastoma Cells |
| title_fullStr | Neuroprotective Effect of Arctigenin via Upregulation of P-CREB in Mouse Primary Neurons and Human SH-SY5Y Neuroblastoma Cells |
| title_full_unstemmed | Neuroprotective Effect of Arctigenin via Upregulation of P-CREB in Mouse Primary Neurons and Human SH-SY5Y Neuroblastoma Cells |
| title_short | Neuroprotective Effect of Arctigenin via Upregulation of P-CREB in Mouse Primary Neurons and Human SH-SY5Y Neuroblastoma Cells |
| title_sort | neuroprotective effect of arctigenin via upregulation of p creb in mouse primary neurons and human sh sy5y neuroblastoma cells |
| topic | arctigenin neuroprotection beta amyloid (Aβ) p-CREB |
| url | http://www.mdpi.com/1422-0067/14/9/18657 |
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