期刊论文详细信息
Journal of Pharmacological Sciences
Serofendic Acid Protects Against Myocardial Ischemia–Reperfusion Injury in Rats
Takeshi Kimura1  Akinori Akaike2  Toshiaki Kume2  Yasuhiko Izumi2  Masashi Kato1  Masaharu Akao1  Moritake Iguchi1  Tadaaki Ioroi2 
[1] Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Japan;Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Japan
关键词: serofendic acid;    myocardial ischemia;    reperfusion;    mitochondrial ATP-sensitive potassium channel;    cardiac myocyte;   
DOI  :  10.1254/jphs.14139FP
学科分类:药学
来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society
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【 摘 要 】

References(38)Cited-By(2)We previously reported that serofendic acid, a lipophilic extract of fetal calf serum, protects against oxidative stress in primary culture of neonatal rat cardiomyocytes. However, the effect of serofendic acid on myocardial ischemia–reperfusion injury in vivo is yet to be determined. In the present study, we investigated the effect of intravenous administration of serofendic acid on ischemia–reperfusion injury induced by transient occlusion of the left coronary artery in rats. The rat heart was subjected to 25-min ischemia followed by 2-h reperfusion. Bolus intravenous administration of serofendic acid (1 �? 10 mg/kg) given twice reduced the infarct volume in a dose-dependent manner. The protective effect of serofendic acid was abolished by pretreatment with 5-hydroxydecanoate, a blocker of mitochondrial ATP-sensitive potassium channels. For further testing of the protective effect of serofendic acid at the subcellular level, we monitored mitochondrial membrane potential (MMP) in individual cells using real-time two-photon imaging of Langendorff-perfused rat heart. A 25-min no-flow ischemia, followed by reperfusion caused progressive MMP loss. Serofendic acid significantly reduced the number of cells undergoing MMP loss. These results suggest that serofendic acid protected cardiac myocytes against myocardial ischemia–reperfusion injury by preserving the functional integrity of mitochondria.

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