Molecules 2013, 18(1), 354-372; doi:10.3390/molecules18010354
Article

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

Meng-Shiou Lee 1,† email, Jung Chao 2,† email, Jiin-Cherng Yen 2 email, Li-Wei Lin 3 email, Fan-Shiu Tsai 3 email, Ming-Tsuen Hsieh 1 email, Wen-Huang Peng 1,* email and Hao-Yuan Cheng 4,* email
1 Department of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, College of Pharmacy, China Medical University, Taichung 402, Taiwan 2 Department and Institute of Pharmacology, National Yang-Ming University, Taipei 112, Taiwan 3 School of Chinese Medicines for Post-Baccalaureate, I-Shou University, Kaohsiung 840, Taiwan 4 Department of Nursing, Chung Jen College of Nursing, Health Sciences and Management, Chiayi 600, Taiwan † These authors contributed equally to this work.
* Authors to whom correspondence should be addressed.
Received: 8 November 2012; in revised form: 21 December 2012 / Accepted: 24 December 2012 / Published: 27 December 2012
(This article belongs to the Section Natural Products)
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Abstract: 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-XL 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-XL 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.
Keywords: glutamate; apoptosis; schizandrin; neuroprotection

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MDPI and ACS Style

Lee, M.-S.; Chao, J.; Yen, J.-C.; Lin, L.-W.; Tsai, F.-S.; Hsieh, M.-T.; Peng, W.-H.; Cheng, H.-Y. Schizandrin Protects Primary Rat Cortical Cell Cultures from Glutamate-Induced Apoptosis by Inhibiting Activation of the MAPK Family and the Mitochondria Dependent Pathway. Molecules 2013, 18, 354-372.

AMA Style

Lee M-S, Chao J, Yen J-C, Lin L-W, Tsai F-S, Hsieh M-T, Peng W-H, Cheng H-Y. Schizandrin Protects Primary Rat Cortical Cell Cultures from Glutamate-Induced Apoptosis by Inhibiting Activation of the MAPK Family and the Mitochondria Dependent Pathway. Molecules. 2013; 18(1):354-372.

Chicago/Turabian Style

Lee, Meng-Shiou; Chao, Jung; Yen, Jiin-Cherng; Lin, Li-Wei; Tsai, Fan-Shiu; Hsieh, Ming-Tsuen; Peng, Wen-Huang; Cheng, Hao-Yuan. 2013. "Schizandrin Protects Primary Rat Cortical Cell Cultures from Glutamate-Induced Apoptosis by Inhibiting Activation of the MAPK Family and the Mitochondria Dependent Pathway." Molecules 18, no. 1: 354-372.

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