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

Tetramethylpyrazine (TMP), 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 w...

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Bibliographic Details
Published in:Life sciences (1973) 2011-04, Vol.88 (17), p.803-809
Main Authors: Gao, Xin, Zhao, Xiao-long, Zhu, Yan-hui, Li, Xiao-mu, Xu, Qiong, Lin, Huan-dong, Wang, Ming-Wei
Format: Article
Language:English
Subjects:
Animals
Antioxidants - pharmacology
Blotting, Western
Cell Line
Glucose - metabolism
Glucose uptake
Membrane Potential, Mitochondrial - drug effects
Mice
Mitochondria, Muscle - drug effects
Mitochondria, Muscle - metabolism
Mitochondrial dysfunction
Muscle
Muscle Fibers, Skeletal - drug effects
Muscle Fibers, Skeletal - metabolism
Oxidative stress
Oxidative Stress - drug effects
Oxygen Consumption - drug effects
Palmitates - antagonists & inhibitors
Palmitates - pharmacology
Pyrazines - pharmacology
Reactive Oxygen Species - metabolism
Reverse Transcriptase Polymerase Chain Reaction
Tetramethylpyrazine
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Summary:Tetramethylpyrazine (TMP), 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. 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-γ coactivator 1 α (PGC1α), 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-[ 3H]glucose uptake. TMP 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 (PGC1α, 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. 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.
ISSN:0024-3205
1879-0631
DOI:10.1016/j.lfs.2011.02.025