Neuroprotective effects of Arctium lappa L. roots against glutamate-induced oxidative stress by inhibiting phosphorylation of p38, JNK and ERK 1/2 MAPKs in PC12 cells

被引:50
|
作者
Tian, Xing [1 ,2 ]
Sui, Shuang [1 ]
Huang, Jin [1 ]
Bai, Jun-Peng [1 ]
Ren, Tian-Shu [2 ]
Zhao, Qing-Chun [1 ,2 ]
机构
[1] Shenyang Pharmaceut Univ, Dept Life Sci & Biochem, Shenyang 110016, Peoples R China
[2] Shenyang Mil Area Command, Gen Hosp, Dept Pharm, Shenyang 110840, Peoples R China
关键词
Arctium lappa; Glutamate; Oxidative stress; Neuroprotection; PC12; cells; INDUCED APOPTOSIS; NEURODEGENERATION; MITOCHONDRIA; TOXICITY; INJURY; MECHANISMS; PATHWAY; SYSTEM; FAMILY; TARGET;
D O I
10.1016/j.etap.2014.05.017
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Many studies have shown that glutamate-induced oxidative stress can lead to neuronal cell death involved in the development of neurodegenerative diseases. In this work, protective effects of ethyl acetate extract (EAE) of Arctium lappa L. roots against glutamate-induced oxidative stress in PC12 cells were evaluated. Also, the effects of EAE on antioxidant system, mitochondrial pathway, and signal transduction pathway were explored. Pretreatment with EAE significantly increased cell viability, activities of GSH-Px and SOD, mitochondrial membrane potential and reduced LDH leakage, ROS formation, and nuclear condensation in a dose-dependent manner. Furthermore, western blot results revealed that EAE increased the Bcl-2/Bax ratio, and inhibited the up-regulation of caspase-3, release of cytochrome c, phosphorylation of p38, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase 1/2 (ERK 1/2). Therefore, our results indicate that EAE may be a promising neuroprotective agent for the prevention and treatment of neurodegenerative diseases implicated with oxidative stress. (C) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:189 / 198
页数:10
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