Inhibitory effects of edaravone on the production of tumor necrosis factor-α in the isolated heart undergoing ischemia and reperfusion

详细信息    查看全文

• 作者：Shunji Onimaru ; Kazuo Nakamura ; Hiroko Kariyazono ; Ryuji Ikeda ; Takayuki Ueno ; Yoshihiro Fukumoto ; Akira Yabuki ; Ryuzo Sakata and Katsushi Yamada
• 关键词：Edaravone ; Tumor necrosis factor ; α ; ; Reperfusion injury ; Adhesion molecule
• 刊名：Heart and Vessels
• 出版年：2006
• 出版时间：March 2006
• 年：2006
• 卷：21
• 期：2
• 页码：108-115
• 全文大小：968 KB
• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Cardiology
  Cardiac Surgery
  Vascular Surgery
  Biomedical Engineering
  Interventional Radiology
  Ultrasound
  
• 出版者：Springer Japan
• ISSN：1615-2573

文摘

We evaluated the effects of edaravone, a hydroxyl radical scavenging agent, on the production of tumor necrosis factor-α (TNF-α) in myocardium, and the release of TNF-α and P-selectin from myocardium after ischemia–reperfusion injury in isolated Langendorff-perfused rat hearts. Cardiodynamic function at stable points during perfusion and 5, 15, 30, and 60 min after the initiation of reperfusion was evaluated by left ventricular developed pressure, rate of increase in left ventricular pressure and rate of decrease in ventricular pressure, coronary flow, and heart rate. At 60 min after the initiation of reperfusion, myocardial infarct size was estimated microscopically using triphenyltetrazolium chloride staining, and expression of TNF-α in myocardium was detected by Western blot and immunohistochemistry. At the same time points as the measurement of cardiodynamic function, TNF-α and the soluble form of P-selectin in coronary effluent were measured by enzyme immunoassay. At all time points during reperfusion, edaravone markedly improved cardiodynamic function and reduced myocardial infarct size in comparison to the control. In myocardium in the control, TNF-α was detected in the endothelial cells and other cells bearing some resemblance to interstitial cells and monocyte cells. Edaravone suppressed this cytokine expression in the corresponding sites. P-selectin as well as TNF-α was found in the coronary effluent of the control, and edaravone significantly decreased soluble P-selectin levels in comparison to the control (P < 0.01). Edaravone might have protective effects on cardiac function through reduction of infarct size via decrease of production of TNF-α in myocardium induced by ischemia–reperfusion injury and through reduction of the release of adhesion molecules such as P-selectin from vascular endothelial cells.