Eucommia ulmoides Oliv. Bark. protects against hydrogen peroxide-induced neuronal cell death in SH-SY5Y cells

被引:37
作者
Kwon, Seung-Hwan [1 ]
Kim, Min-Jung [1 ]
Ma, Shi-Xun [1 ]
You, In-Jee [1 ]
Hwang, Ji-Young [1 ]
Oh, Ji-Hwan [1 ]
Kim, Sun-Yeou [2 ]
Kim, Hyoung-Chun [3 ]
Lee, Seok-Yong [1 ]
Jang, Choon-Gon [1 ]
机构
[1] Sungkyunkwan Univ, Dept Pharmacol, Sch Pharm, Suwon 440746, South Korea
[2] Gachon Univ Med & Sci, Dept Pharmacol, Sch Pharm, Inchon 406840, South Korea
[3] Kangwon Natl Univ, Neurotoxicol Program, Coll Pharm, Korea Inst Drug Abuse, Chunchon 200701, South Korea
关键词
Eucommia ulmoides Oliv. Bark; Hydrogen peroxide; Neuronal cell death; Neurodegenerative diseases; Alzheimer's disease; ANTIOXIDANT ENZYME-ACTIVITY; OXIDATIVE STRESS; INDUCED APOPTOSIS; REACTIVE OXYGEN; SIGNALING PATHWAYS; CHLOROGENIC ACID; WATER EXTRACT; PC12; CELLS; PHOSPHORYLATION; ACTIVATION;
D O I
10.1016/j.jep.2012.04.010
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Ethnopharmacological relevance: Eucommia ulmoides Oliv. Bark. (EUE), has commonly been used to fortify the muscles and lungs, lower blood pressure, prevent miscarriage, improve the tone of liver and kidneys, and promote longevity the traditional tonic medicines of Korea, China, and Japan. Aim of the study: In this study, we investigated that the neuroprotective activities and possible mechanisms of EUE aqueous extract in hydrogen peroxide (H2O2)-induced neuronal cell death in human SH-SY5Y neuroblastoma cells. Material and method: We examined the effects of EUE against H2O2-induced cytotoxicity, DNA condensation, the production of reactive oxygen species (ROS), loss of mitochondria membrane potential (MMP), the proteolysis of cleaved poly-ADP-ribose polymerase (PARP), and the expression of Bcl-2, Bcl-xL, cleaved caspase-3, and release of cytochrome c. Moreover, we attempted to determine whether EUE suppressed the phosphorylation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase 1/2 (ERK 1/2), and phosphoinositide 3-kinase (PI3K)/Akt. Results: Pretreatment with EUE increased cell viability and inhibited cytotoxicity and DNA condensation. EUE also attenuated the increase in ROS production and MMP reduction. Western blot data revealed that EUE inhibited H2O2-induced up- or down-regulation of cleaved PARP, cleaved caspase-3, Bcl-2, and Bcl-xL. The EUE inhibited release of cytochrome c from mitochondria to the cytosol, and significantly attenuated H2O2-induced phosphorylation of JNK, p38 MAPK, ERK 1/2, and PI3K/Akt. Conclusion: The potent neuroprotective capacity of EUE, shown in these experiments. may potentially be applied in the prevention or treatment of neurodegenerative diseases such as Alzheimer's disease (AD). (C) 2012 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:337 / 345
页数:9
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