Ac-cel, a Novel Antioxidant, Protects Against Hydrogen Peroxide-induced Injury in PC12 Cells via Attenuation of Mitochondrial Dysfunction
文献类型:期刊论文
作者 | Guo, Xianjun; Chen, Yuting; Liu, Qunfang![]() ![]() ![]() ![]() |
刊名 | JOURNAL OF MOLECULAR NEUROSCIENCE
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出版日期 | 2013-07 |
卷号 | 50期号:3页码:453-461 |
关键词 | Apoptosis Antioxidant Hydrogen peroxide Mitochondria Neuroprotection Reactive oxygen species |
ISSN号 | 0895-8696 |
DOI | 10.1007/s12031-013-9955-1 |
文献子类 | Article |
英文摘要 | Oxidative stress has been implicated in pathophysiology of many neurodegenerative diseases (ND) and increased oxidative stress is closely associated with mitochondrial dysfunction. As a result, looking for potent antioxidants, especially those targeting mitochondria, has become an attractive strategy in ND therapy. In this study, we explored protective effects and potential mechanism of Ac-cel, a novel compound, against hydrogen peroxide (H2O2)-induced injury in PC12 cells. Pretreatment of PC12 cells with Ac-cel prior to 24 h of H2O2 exposure markedly attenuated cytotoxicity induced by H2O2 as evidenced by morphological changes and 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Ac-cel also exhibited potent antiapoptotic effect demonstrated by results of annexin V and PI staining. The above beneficial effects of Ac-cel were accompanied by improved mitochondrial function, reduced caspase-3 cleavage as well as upregulated ratio of Bcl-2/Bax protein expression. Moreover, Ac-cel pretreatment markedly reversed intracellular reactive oxygen species (ROS) accumulation following 30 min of H2O2 exposure in PC12 cells. Further, subcellular investigation indicated that Ac-cel significantly reduced production of mitochondrial ROS in isolated rat cortical mitochondria. Taken together, the present study, for the first time, reports that Ac-cel pretreatment inhibits H2O2-stimulated early accumulation of intracellular ROS possibly via reducing mitochondrial ROS production directly and leads to subsequent preservation of mitochondrial function. These results indicate that Ac-cel is a potential drug candidate for treatment of oxidative stress-associated ND. |
WOS关键词 | INDUCED OXIDATIVE DAMAGE ; ACETYLCHOLINESTERASE INHIBITOR ; FREE-RADICALS ; CYTOCHROME-C ; DNA-DAMAGE ; APOPTOSIS ; STRESS ; BRAIN ; HUPERZINE ; PATHWAYS |
资助项目 | Ministry of Science and Technology of China[2011CB510004] ; National Natural Science Foundation of China[81173034] ; National Natural Science Foundation of China[81072646] ; National Science & Technology Major Project "Key New Drug Creation and Manufacturing Program" of China[2012ZX09301001-001] ; National Science & Technology Major Project "Key New Drug Creation and Manufacturing Program" of China[2012ZX09301001-004] ; SKLDR/SIMM Projects[SIMM1105KF-04] ; SKLDR/SIMM Projects[SIMM1203KF-02] ; Shanghai Science and Technology Development Funds, SA-SIBS Scholarship Program[10QA1408100] |
WOS研究方向 | Biochemistry & Molecular Biology ; Neurosciences & Neurology |
语种 | 英语 |
WOS记录号 | WOS:000320048400008 |
出版者 | HUMANA PRESS INC |
源URL | [http://119.78.100.183/handle/2S10ELR8/277573] ![]() |
专题 | 天然药物化学研究室 中科院受体结构与功能重点实验室 新药研究国家重点实验室 药理学第二研究室 |
通讯作者 | Zhao, Weimin |
作者单位 | Chinese Acad Sci, State Key Lab Drug Res, Shanghai Inst Mat Med, Shanghai 201203, Peoples R China |
推荐引用方式 GB/T 7714 | Guo, Xianjun,Chen, Yuting,Liu, Qunfang,et al. Ac-cel, a Novel Antioxidant, Protects Against Hydrogen Peroxide-induced Injury in PC12 Cells via Attenuation of Mitochondrial Dysfunction[J]. JOURNAL OF MOLECULAR NEUROSCIENCE,2013,50(3):453-461. |
APA | Guo, Xianjun.,Chen, Yuting.,Liu, Qunfang.,Wu, Jian.,Wang, Luoyi.,...&Zhang, Haiyan.(2013).Ac-cel, a Novel Antioxidant, Protects Against Hydrogen Peroxide-induced Injury in PC12 Cells via Attenuation of Mitochondrial Dysfunction.JOURNAL OF MOLECULAR NEUROSCIENCE,50(3),453-461. |
MLA | Guo, Xianjun,et al."Ac-cel, a Novel Antioxidant, Protects Against Hydrogen Peroxide-induced Injury in PC12 Cells via Attenuation of Mitochondrial Dysfunction".JOURNAL OF MOLECULAR NEUROSCIENCE 50.3(2013):453-461. |
入库方式: OAI收割
来源:上海药物研究所
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