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Myricitrin Alleviates Methylglyoxal-Induced Mitochondrial Dysfunction and AGEs/RAGE/NF-kappa B Pathway Activation in SH-SY5Y Cells
Wang, Yue-Hua1,2,3,4,5; Yu, Hai-Tao6; Pu, Xiao-Ping1,2; Du, Guan-Hua3,4,5
关键词Myricitrin Methylglyoxal (MGO) Advanced glycation end products (AGEs) Mitochondria SH-SY5Y cells
刊名JOURNAL OF MOLECULAR NEUROSCIENCE
2014-08-01
DOI10.1007/s12031-013-0222-2
53期:4页:562-570
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Neurosciences
研究领域[WOS]Biochemistry & Molecular Biology ; Neurosciences & Neurology
关键词[WOS]GLYCATION END-PRODUCTS ; IN-VITRO ; OXIDATIVE STRESS ; PC12 CELLS ; ALZHEIMERS-DISEASE ; PHENOLIC-ACIDS ; UP-REGULATION ; PROTEINS ; RAGE ; RECEPTOR
英文摘要

Advanced glycation end products (AGEs) have been identified in age-related intracellular protein deposits of neurodegenerative diseases. Methylglyoxal (MGO), a dicarbonyl metabolite, is a major precursor of AGEs which have been linked to the development of neurodegenerative diseases. Myricitrin, a flavanoid isolated from the root bark of Myrica cerifera, attenuated 6-OHDA-induced mitochondrial dysfunction and had a potential anti-Parkinson′s disease in our previous investigation. The aims of this study were to investigate the protective effects of myricitrin against MGO-induced injury in SH-SY5Y cells and also to look for the possible mechanisms. The results showed that exposure of SH-SY5Y cells to MGO caused decreases of cell viability, intracellular ATP, mitochondrial redox activity, and mitochondrial membrane potential and an increase in reactive oxygen species generation. However, these mitochondrial dysfunctions were alleviated by co-treatment with myricitrin. Additionally, myricitrin was capable of inhibiting AGEs formation, blocking RAGE expression, and inhibiting NF-kappa B activation and translocation triggered by MGO in SH-SY5Y cells. Our results suggest that myricitrin alleviates MGO-induced mitochondrial dysfunction, and the possible mechanism is through modulating the AGEs/RAGE/NF-kappa B pathway. In summary, myricitrin might offer a promising therapeutic strategy to reduce the neurotoxicity of reactive dicarbonyl compounds, providing a potential benefit agent with age-related neurodegenerative diseases.

语种英语
WOS记录号WOS:000340473300004
项目编号30973889 ; 2012ZX09103101-078 ; 2012ZX09103201-042 ; 2011ZX09401-014 ; 200902008
资助机构National Natural Science Foundation of China ; Science and Technology Major Projects: significant new-drugs creation ; Research Special Fund for Public Welfare Industry of Health
引用统计
被引频次:17[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/63818
专题北京大学药学院
北京大学药学院_分子与细胞药理学系
作者单位1.Jiangsu Kanon Pharmaceut Co Ltd, Lianyungang, Jiangsu, Peoples R China
2.Peking Univ, Natl Key Res Lab Nat & Biomimet Drugs, Beijing 100871, Peoples R China
3.Peking Univ, Sch Pharmaceut Sci, Dept Mol & Cellular Pharmacol, Beijing 100871, Peoples R China
4.Chinese Acad Med Sci, Inst Mat Med, Beijing Key Lab Drug Target Identificat, Beijing 100050, Peoples R China
5.Peking Union Med Coll, Beijing 100021, Peoples R China
6.Chinese Acad Med Sci, Inst Mat Med, State Key Lab Bioact Subst & Funct Nat Med, Beijing 100050, Peoples R China
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Wang, Yue-Hua,Yu, Hai-Tao,Pu, Xiao-Ping,et al. Myricitrin Alleviates Methylglyoxal-Induced Mitochondrial Dysfunction and AGEs/RAGE/NF-kappa B Pathway Activation in SH-SY5Y Cells[J]. JOURNAL OF MOLECULAR NEUROSCIENCE,2014,53(4):562-570.
APA Wang, Yue-Hua,Yu, Hai-Tao,Pu, Xiao-Ping,&Du, Guan-Hua.(2014).Myricitrin Alleviates Methylglyoxal-Induced Mitochondrial Dysfunction and AGEs/RAGE/NF-kappa B Pathway Activation in SH-SY5Y Cells.JOURNAL OF MOLECULAR NEUROSCIENCE,53(4),562-570.
MLA Wang, Yue-Hua,et al."Myricitrin Alleviates Methylglyoxal-Induced Mitochondrial Dysfunction and AGEs/RAGE/NF-kappa B Pathway Activation in SH-SY5Y Cells".JOURNAL OF MOLECULAR NEUROSCIENCE 53.4(2014):562-570.
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