Inhibition of semicarbazide-sensitive amine oxidase attenuates myocardial ischemia–reperfusion injury in an in vivo rat model

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• 作者：Wei Yang^a ; Hui Li^a ; Hongjun Luo^a ; Wenhong Luo ; ^a ; ^{whluo@stu.edu.cn}
• 关键词：Semicarbazide-sensitive amine oxidase ; Inflammation ; Ischemia-reperfusion injury
• 刊名：Life Sciences
• 出版年：2011
• 出版时间：14 February 2011
• 年：2011
• 卷：88
• 期：7-8
• 页码：302-306
• 全文大小：632 K

文摘

Aims

This study tested the hypothesis that the inhibition of semicarbazide-sensitive amine oxidase (SSAO) after ischemia could attenuate myocardial ischemia–reperfusion (I/R) injury.

Main methods

Anesthetized male Sprague–Dawley rats underwent myocardial I/R injury. Saline, semicarbazide (SCZ, 30 mg/kg), hydralazine (HYD, 10 mg/kg), or LJP 1207 (30 mg/kg) was administered intraperitoneally 3 min before reperfusion. After 30 min of ischemia and 180 min of reperfusion, the myocardial infarct size was determined using nitroblue tetrazolium staining. Myocardial myeloperoxidase activity was determined through biochemical assay. HE staining was used for histopathological evaluation. Myocardial SSAO activity was assayed with high performance liquid chromatography analysis. Additionally, the endothelial expression of P-selectin was evaluated using immunohistochemistry after 30 min of ischemia and 20 min of reperfusion.

Key findings

Myocardial SSAO activity was increased in myocardial I/R injury. Administration of SCZ, HYD, or LJP 1207 reduced the myocardial infarct size and decreased leukocyte infiltration and endothelial P-selectin expression in myocardial I/R injury in vivo.

Significance

These data suggest that myocardial I/R injury up-regulates myocardial SSAO activity, and the inhibition of SSAO prior to reperfusion is able to attenuate acute myocardial I/R injury.