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Schizandrin Protects Primary Rat Cortical Cell Cultures from Glutamate-Induced Apoptosis by Inhibiting Activation of the MAPK Family and the Mitochondria Dependent Pathway

Glutamate-induced excitotoxicity has been implicated in a variety of neuronal degenerative disorders. In the present study, we investigated the possible neuroprotective effects of schizandrin against apoptosis of primary cultured rat cortical cells induced by glutamate. Glutamate (10 μM) administere...

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Autores principales: Lee, Meng-Shiou, Chao, Jung, Yen, Jiin-Cherng, Lin, Li-Wei, Tsai, Fan-Shiu, Hsieh, Ming-Tsuen, Peng, Wen-Huang, Cheng, Hao-Yuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6270204/
https://www.ncbi.nlm.nih.gov/pubmed/23271470
http://dx.doi.org/10.3390/molecules18010354
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author Lee, Meng-Shiou
Chao, Jung
Yen, Jiin-Cherng
Lin, Li-Wei
Tsai, Fan-Shiu
Hsieh, Ming-Tsuen
Peng, Wen-Huang
Cheng, Hao-Yuan
author_facet Lee, Meng-Shiou
Chao, Jung
Yen, Jiin-Cherng
Lin, Li-Wei
Tsai, Fan-Shiu
Hsieh, Ming-Tsuen
Peng, Wen-Huang
Cheng, Hao-Yuan
author_sort Lee, Meng-Shiou
collection PubMed
description Glutamate-induced excitotoxicity has been implicated in a variety of neuronal degenerative disorders. In the present study, we investigated the possible neuroprotective effects of schizandrin against apoptosis of primary cultured rat cortical cells induced by glutamate. Glutamate (10 μM) administered for 24 h decreased the expression of Bcl-2 and Bcl-X(L) protein, whereas increased the expression of Bax, Bak, apoptosis inducing factor (AIF), endonuclease G (Nodo G) and endoplasmic reticulum (ER) stress of caspase-12. Pretreatment with schizandrin (100 μM) before glutamate treatment increased the Bcl-X(L) and Bcl-2 expression and decreased Bax, Bak, AIF, Nodo G and caspase-12 compared with those only treated with glutamate. Furthermore, glutamate-induced phosphorylation of JNK, p38 and ERK mitogen-activated protein kinases (MAPK), and these effects were attenuated by schizandrin (100 μM) treatment. These results suggest that schizandrin possesses the neuroprotective effects. The molecular mechanisms of schizandrin against glutamate-induced apoptosis may involve the regulation of Bcl-2 family proteins expression, and ER stress through blocking the activation of JNK, ERK and p38 MAPK.
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spelling pubmed-62702042018-12-14 Schizandrin Protects Primary Rat Cortical Cell Cultures from Glutamate-Induced Apoptosis by Inhibiting Activation of the MAPK Family and the Mitochondria Dependent Pathway Lee, Meng-Shiou Chao, Jung Yen, Jiin-Cherng Lin, Li-Wei Tsai, Fan-Shiu Hsieh, Ming-Tsuen Peng, Wen-Huang Cheng, Hao-Yuan Molecules Article Glutamate-induced excitotoxicity has been implicated in a variety of neuronal degenerative disorders. In the present study, we investigated the possible neuroprotective effects of schizandrin against apoptosis of primary cultured rat cortical cells induced by glutamate. Glutamate (10 μM) administered for 24 h decreased the expression of Bcl-2 and Bcl-X(L) protein, whereas increased the expression of Bax, Bak, apoptosis inducing factor (AIF), endonuclease G (Nodo G) and endoplasmic reticulum (ER) stress of caspase-12. Pretreatment with schizandrin (100 μM) before glutamate treatment increased the Bcl-X(L) and Bcl-2 expression and decreased Bax, Bak, AIF, Nodo G and caspase-12 compared with those only treated with glutamate. Furthermore, glutamate-induced phosphorylation of JNK, p38 and ERK mitogen-activated protein kinases (MAPK), and these effects were attenuated by schizandrin (100 μM) treatment. These results suggest that schizandrin possesses the neuroprotective effects. The molecular mechanisms of schizandrin against glutamate-induced apoptosis may involve the regulation of Bcl-2 family proteins expression, and ER stress through blocking the activation of JNK, ERK and p38 MAPK. MDPI 2012-12-27 /pmc/articles/PMC6270204/ /pubmed/23271470 http://dx.doi.org/10.3390/molecules18010354 Text en © 2013 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Article
Lee, Meng-Shiou
Chao, Jung
Yen, Jiin-Cherng
Lin, Li-Wei
Tsai, Fan-Shiu
Hsieh, Ming-Tsuen
Peng, Wen-Huang
Cheng, Hao-Yuan
Schizandrin Protects Primary Rat Cortical Cell Cultures from Glutamate-Induced Apoptosis by Inhibiting Activation of the MAPK Family and the Mitochondria Dependent Pathway
title Schizandrin Protects Primary Rat Cortical Cell Cultures from Glutamate-Induced Apoptosis by Inhibiting Activation of the MAPK Family and the Mitochondria Dependent Pathway
title_full Schizandrin Protects Primary Rat Cortical Cell Cultures from Glutamate-Induced Apoptosis by Inhibiting Activation of the MAPK Family and the Mitochondria Dependent Pathway
title_fullStr Schizandrin Protects Primary Rat Cortical Cell Cultures from Glutamate-Induced Apoptosis by Inhibiting Activation of the MAPK Family and the Mitochondria Dependent Pathway
title_full_unstemmed Schizandrin Protects Primary Rat Cortical Cell Cultures from Glutamate-Induced Apoptosis by Inhibiting Activation of the MAPK Family and the Mitochondria Dependent Pathway
title_short Schizandrin Protects Primary Rat Cortical Cell Cultures from Glutamate-Induced Apoptosis by Inhibiting Activation of the MAPK Family and the Mitochondria Dependent Pathway
title_sort schizandrin protects primary rat cortical cell cultures from glutamate-induced apoptosis by inhibiting activation of the mapk family and the mitochondria dependent pathway
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6270204/
https://www.ncbi.nlm.nih.gov/pubmed/23271470
http://dx.doi.org/10.3390/molecules18010354
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