Silibinin Protects Against Isoproterenol-Induced Rat Cardiac Myocyte Injury Through Mitochondrial Pathway After Up-regulation of SIRT1
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概要
- 論文の詳細を見る
Terminally differentiated adult injured cardiac myocytes have been used for various animal models of heart failure. It has recently been shown that isoproterenol induces injury in rat neonatal cardiac myocytes via a β-adrenergic pathway, suggesting that it might be one of the factors involved in myocardial cell injury in heart failure in vivo. In the study, silibinin, a plant flavanoid from milk thistle was first evaluated for its protective effect against β-adrenergic agonist isoproterenol-induced injury in cultured rat neonatal cardiac myocytes. The viability, activation of lactate dehydrogenase (LDH), and content of maleic dialdehyde (MDA) were chosen for measuring the degree of cardiac myocytes injury. As a result, silibinin protected isoproterenol-treated rat cardiac myocytes from death and significantly decreased LDH release and MDA production. Silibinin increased superoxide dismutase activity, decreased [Ca2+]i, and increased mitochondrial membrane potential (ΔΨ). Furthermore, the release of pro-apoptotic cytochrome c from mitochondria was reduced by silibinin. Silibinin increased the expression of anti-apoptotic Bcl-2 family protein Bcl-2, and up-regulation of SIRT1 inhibited the translocation of Bax from cytoplasm to mitochondria, which caused mitochondrial dysfunction and cell injury. These results demonstrate that silibinin protects against isoproterenol-induced cardiac myocytes injury through resuming mitochondrial function and regulating the expression of SIRT1 and Bcl-2 family members.
- 社団法人 日本薬理学会の論文
- 2006-12-20
著者
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Tashiro Shin-ichi
Dep. Of Clinical And Biomedical Sciences Showa Pharmaceutical Univ. Jpn
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TASHIRO Shin-ichi
Department of Clinical and Biomedical Sciences, Showa Pharmaceutical University
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ONODERA Satoshi
Department of Clinical and Biomedical Sciences, Showa Pharmaceutical University
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IKEJIMA Takashi
China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical Unive
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Wu Li-jun
Department Of Phytochemistry Shenyang Pharmaceutical University
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Wu L
Department Of Phytochemistry Shenyang Pharmaceutical University
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Onodera S
Dep. Of Clinical And Biomedical Sciences Showa Pharmaceutical Univ. Jpn
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Onodera Satoshi
昭和薬科大学 病態科
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Ikejima Takashi
China-japan Res. Inst. Of Medical And Pharmaceutical Sciences Shenyang Pharmaceutical Univ. Chn
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ZHOU Bei
China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical Unive
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LI Lin-Hao
China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical Unive
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UCHIUMI Fumiaki
Department of Gene Regulation, Faculty of Pharmaceutical Sciences, Tokyo University of Science
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Tashiro Shin-ichi
Department Of Clinical And Biomedical Sciences Showa Pharmaceutical University
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Onodera Satoshi
Department Of Cinical And Biomedical Sciences Showa Pharmaceutical University
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Tashiro Shin-ichi
Department Of Cinical And Biomedical Sciences Showa Pharmaceutical University
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Li Lin-hao
China-japan Research Institute Of Medical And Pharmaceutical Sciences Shenyang Pharmaceutical Univer
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Uchiumi Fumiaki
Department Of Gene Regulation Faculty Of Pharmaceutical Sciences Tokyo University Of Science
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Uchiumi Fumiaki
Department Of Biochemistry Faculty Of Pharmaceutical Sciences Tokyo University Of Science
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Tashiro S
Department Of Clinical And Biomedical Sciences Showa Pharmaceutical University
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Onodera S
Department Of Clinical And Biomedical Sciences Showa Pharmaceutical University
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Zhou Bei
China-japan Research Institute Of Medical And Pharmaceutical Sciences Shenyang Pharmaceutical Univer
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Ikejima Takashi
China–Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University
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