马学虎

个人信息Personal Information

教授

博士生导师

硕士生导师

性别:男

毕业院校:大连理工大学

学位:博士

所在单位:化工学院

学科:化学工程. 工程热物理

办公地点:化工学院 化工实验楼 D-309

联系方式:辽宁省大连市凌工路2号 大连理工大学化环生学部化工学院 116024

电子邮箱:xuehuma@dlut.edu.cn

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Pyrroloquinoline quinone against glutamate-induced neurotoxicity in cultured neural stem and progenitor cells

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论文类型:期刊论文

发表时间:2015-05-01

发表刊物:INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE

收录刊物:SCIE、PubMed、Scopus

卷号:42

页面范围:37-45

ISSN号:0736-5748

关键字:Pyrroloquinoline quinone; Neural stem and progenitor cells; Glutamate; Reactive oxygen species; Neuroprotection

摘要:Pyrroloquinoline quinone (PQQ), as a well-known redox enzyme cofactor, has been proven to play important roles in the regulation of cellular growth and development in mammals. Numerous physiological and medicinal functions of PQQ have so far been reported although its effect on neural stem and progenitor cells (NS/PCs) and the potential mechanism were even rarely investigated. In this study, the neuroprotective effects of PQQ were observed by pretreatment of NS/PCs with PQQ before glutamate injury, and the possible mechanisms were examined. PQQ stimulated cell proliferation and markedly attenuated glutamate-induced cell damage in a dose-dependent manner. By observing the nuclear morphological changes and flow cytometric analysis, PQQ pretreatment showed its significant effect on protecting NS/PCs against glutamate-induced apoptosis/necrosis. PQQ neuroprotection was associated with the decrease of intracellular reactive oxygen species (ROS) production, the increase of glutathione (GSH) levels, and the decrease of caspase-3 activity. In addition, pretreatment with PQQalso significantly enhanced the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) in the NS/PCs exposed to glutamate. These results suggest that PQQ can protect NS/PCs against glutamate toxicity associated with ROS-mediated mitochondrial pathway, indicating a useful chemical for the clinical application of NS/PCs. (C) 2015 Elsevier Ltd. All rights reserved.