Tetramethylpyrazine protects palmitate-induced oxidative damage and mitochondrial dysfunction in C2C12 myotubes

doi:10.1016/j.lfs.2011.02.025

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	Tetramethylpyrazine protects palmitate-induced oxidative damage and mitochondrial dysfunction in C2C12 myotubes
	Gao, Xin 1; Zhao, Xiao-long 2; Zhu, Yan-hui 3; Li, Xiao-mu 1; Xu, Qiong 1; Lin, Huan-dong 1; Wang, Ming-Wei3
刊名	LIFE SCIENCES
	2011-04-25
卷号	88 期号:17-18 页码:803-809
关键词	Muscle Tetramethylpyrazine Oxidative stress Mitochondrial dysfunction Glucose uptake
ISSN号	0024-3205
DOI	10.1016/j.lfs.2011.02.025
文献子类	Article
英文摘要	Aims: Tetramethylpyrazine (IMP), one of the active ingredients isolated from a Chinese herbal prescription, possesses protective effects against oxidative stress caused by high glucose in endothelial cells. In this study, the role of TMP in preventing muscle cells from palmitate-induced oxidative damage was investigated and the possible mechanisms of action elucidated. Main methods: Mitochondrial reactive oxygen species (ROS) were measured in C2C12 myotubes, a palmitate-induced oxidative stress cell model, with or without TMP. Both mitochondrial membrane potential (MMP) and oxygen consumption were assessed in conjunction with quantification of mitochondrial DNA and mitochondrial biogenesis-related factors, such as peroxisome proliferator-activated receptor-gamma coactivator 1 (PGC1 alpha), nuclear respiratory factor 1 (NRF1) and mitochondrial transcription factor A (Tfam), by real-time polymerase chain reaction. Expression of mitochondrial respiratory chain complex III as an index of mitochondrial function was evaluated by immunoblotting, and glucose transport into the C2C12 myotube examined by analyzing 2-deoxy-[(3)H]glucose uptake. Key findings: IMP significantly alleviated palmitate-induced mitochondrial ROS production, mitigated mitochondrial dysfunction and increased D-loop mRNA expression as compared with the control. This was accompanied by a marked reversal of palmitate-induced down-regulation in the expression of mitochondrial biogenesis-related factors (PGC1 alpha, NRF1 and Tfam) and decreased glucose uptake in C2C12 myotubes. As a result, cell respiration, as reflected by the elevated expression of mitochondrial respiratory chain complex III and oxygen consumption, was enhanced. Significance: TMP is capable of protecting C2C12 myotubes against palmitate-induced oxidative damage and mitochondrial dysfunction, and improving glucose uptake in muscle cells partially through the up-regulation of mitochondrial biogenesis. (C) 2011 Elsevier Inc. All rights reserved.
资助项目	National Science Foundation of China[30871196] ; National Science Foundation of China[30700385] ; Ministry of Science and Technology of China[2009ZX09302-001] ; Shanghai Municipality Government[08DZ2291300] ; Shanghai Municipality government[09DZ2291200]
WOS关键词	HUMAN SKELETAL-MUSCLE ; INSULIN-RESISTANCE ; ENDOTHELIAL-CELLS ; FACTOR-I ; ACID ; GLUCOSE ; SPECTROSCOPY ; PGC-1-ALPHA ; METABOLISM ; OBESITY
WOS研究方向	Research & Experimental Medicine ; Pharmacology & Pharmacy
语种	英语
出版者	PERGAMON-ELSEVIER SCIENCE LTD
WOS记录号	WOS:000289922800010
内容类型	期刊论文
源URL	[http://119.78.100.183/handle/2S10ELR8/278553]
专题	国家新药筛选中心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
通讯作者	Gao, Xin
作者单位	1.Fudan Univ, Zhongshan Hosp, Dept Endocrinol & Metab, Shanghai 200032, Peoples R China; 2.Fudan Univ, Huashan Hosp, Dept Endocrinol & Metab, Shanghai 200040, Peoples R China; 3.Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Natl Ctr Drug Screening, Shanghai 201203, Peoples R China
推荐引用方式 GB/T 7714	Gao, Xin,Zhao, Xiao-long,Zhu, Yan-hui,et al. Tetramethylpyrazine protects palmitate-induced oxidative damage and mitochondrial dysfunction in C2C12 myotubes[J]. LIFE SCIENCES,2011,88(17-18):803-809.
APA	Gao, Xin.,Zhao, Xiao-long.,Zhu, Yan-hui.,Li, Xiao-mu.,Xu, Qiong.,...&Wang, Ming-Wei.(2011).Tetramethylpyrazine protects palmitate-induced oxidative damage and mitochondrial dysfunction in C2C12 myotubes.LIFE SCIENCES,88(17-18),803-809.
MLA	Gao, Xin,et al."Tetramethylpyrazine protects palmitate-induced oxidative damage and mitochondrial dysfunction in C2C12 myotubes".LIFE SCIENCES 88.17-18(2011):803-809.