Shengmai-san Enhances Antioxidant Potential in C2C12 Myoblasts Through the Induction of Intracellular Glutathione Peroxidase
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- Nishida Hiroshi
- Department of Applied Life Sciences, Niigata University of Pharmacy and Applied Life Sciences, Japan
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- Ichikawa Haruyo
- Department of Applied Life Sciences, Niigata University of Pharmacy and Applied Life Sciences, Japan
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- Konishi Tetsuya
- Department of Applied Life Sciences, Niigata University of Pharmacy and Applied Life Sciences, Japan
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説明
Cellular and tissue injury associated with reactive oxygen species (ROS) has been reported in many kinds of disorders. While the antioxidant enzymes play critical roles in inhibiting the ROS-mediated injury, glutathione peroxidase (GPx) is scavenging hydroperoxides including H2O2. We previously reported that Shengmai-san (SMS), a traditional Chinese medicine, prevented ischemia/reperfusion injury of the brain and other organs in rats. To clarify the effect of SMS on intracellular responses of muscle cells against oxidative stress, C2C12 myoblasts were subjected to H2O2 abuse. SMS pre-incubation prevented the decreasing cell viability after H2O2 treatment. The accumulations of cellular protein carbonyl associated with apoptotic cell death were also inhibited by the SMS pre-incubation prior to oxidative damage induction. At the same time, enhanced activity, protein, and mRNA expression levels of GPx were observed in cells pre-incubated with SMS prior to H2O2 abuse. Moreover, intracellular GSH was subsequently decreased after H2O2 treatment. These findings suggest that SMS improved the antioxidant capacity against acute oxidative stress through the constitutive enhancement of GPx expression in C2C12 myoblasts. Because of its antioxidative property, SMS might be useful not only for the oxidative damage associated diseases but also for the transplantation of myoblasts into muscular dystrophy patients.<br>
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 105 (4), 342-352, 2007
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390001205181054464
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- NII論文ID
- 10024317066
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- NII書誌ID
- AA11806667
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 9314449
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
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