Neuroprotective effects of Psoralea corylifolia Linn seed extracts on mitochondrial dysfunction induced by 3-nitropropionic acid

BMC Complementary and Alternative Medicine

Research Article

Sung-Wook Chae¹  Mi-Young Lee¹  A-Rang Im¹  Gui jun Zhang² 

[1]KM-Based Herbal Drug Development Group, Korea Institute of Oriental Medicine, 1672 Yuseongdae-ro, 305-811, Yuseong-gu, Daejeon, South Korea

[2]School of Chinese Materia Medica, Beijing University of Chinese Medicine, 100102, Beijing, China

关键词: Psoralea corylifolia;    3-nitropropionic acid;    Mitochondrial dysfunction;    Cellular bioenergetics;   

DOI  :  10.1186/1472-6882-14-370

 received in 2014-05-07, accepted in 2014-09-29,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundMitochondrial dysfunction has been implicated in neuronal apoptosis associated with neurodegenerative diseases such as Huntington’s disease (HD). Animals that are administered 3-nitropropionic acid (3-NP), a mitochondrial toxin that specifically inhibits complex II of the mitochondrial electron transport chain, manifest HD-like symptoms.MethodsPsoralea corylifolia Linn seed extracts against 3-NP induced mitochondrial dysfunction in cultured rat pheochromocytoma (PC12) cells, which are used for neurobiological studies.ResultsIn this study showed that 3-NP-treated PC12 cells had decreased ATP levels, lower cellular oxygen consumption, and reduced mitochondrial membrane potential than those of untreated PC12 cells. Psoralea corylifolia Linn seed extracts stimulated mitochondrial respiration with uncoupling and induced an increased bioenergetic reserve capacity. Furthermore, PC12 cells pretreated with P. corylifolia Linn seed extracts significantly attenuated 3-NP-induced cell death, reduced ATP levels, and lowered the mitochondrial membrane potential.ConclusionsThese results demonstrate that P. corylifolia Linn seed extracts have a significant protective effect against 3-NP induced cytotoxicity. Thus, our results indicate that P. corylifolia Linn seed extracts may have potential applications as therapeutic agents for treating neurodegenerative disease.

【 授权许可】

Unknown   
© Im et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.