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学科主题: 药学
题名:
Myricitrin Alleviates Methylglyoxal-Induced Mitochondrial Dysfunction and AGEs/RAGE/NF-kappa B Pathway Activation in SH-SY5Y Cells
作者: 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
发表日期: 2014-08-01
DOI: 10.1007/s12031-013-0222-2
卷: 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
所属项目编号: 30973889 ; 2012ZX09103101-078 ; 2012ZX09103201-042 ; 2011ZX09401-014 ; 200902008
项目资助者: National Natural Science Foundation of China ; Science and Technology Major Projects: significant new-drugs creation ; Research Special Fund for Public Welfare Industry of Health
WOS记录号: WOS:000340473300004
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内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/63818
Appears in Collections:北京大学药学院_期刊论文

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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

Recommended Citation:
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.
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