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Sustained protective effects of 7-monohydroxyethylrutoside in an in vivo model of cardiac ischemia-reperfusion

De Celle, T., Heeringa, P., Strzelecka, AE., Bast, A., Smits, JF. & Janssen, BJ., 28-Jun-2004, In : European Journal of Pharmacology. 494, 2-3, p. 205-212 8 p.

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  • T De Celle
  • P Heeringa
  • AE Strzelecka
  • A Bast
  • JF Smits
  • BJ Janssen

Earlier studies have shown that 7-monohydroxyethylrutoside (monoHER), an antioxidant flavonoid, protects against doxorubicin-induced cardiotoxicity. In this study, we investigated potential sustained cardioprotective effects of monoHER in a model of ischemia-reperfusion (I/R) in mice. Ischemia was induced for 30 min by ligating the left anterior descending coronary artery. Afterwards, the ligature was removed and reperfusion was allowed for 6 or 24 h or 2 weeks. MonoHER (500 mg/kg) was given intraperitoneally (i.p.) one hour before ischemia. Treatment with monoHER significantly attenuated myocardial neutrophil influx both at 6 and 24 h after reperfusion by 77% and 76%, respectively. Infarct size was also significantly reduced, 24 h and 2 weeks after reperfusion by 58% and 49%, respectively. Whereas ischemia-reperfusion had no influence on basal levels of cardiac contractility (+dp/dt), responses to dobutamine were blunted 24 h and 2 weeks after reperfusion. In mice treated with monoHER, cardiac contractility response was significantly restored. These results indicate that monoHER exerts a sustained cardioprotective effect on ischemia-reperfusion injury and prevents deterioration of cardiac contractility. (C) 2004 Elsevier B.V. All rights reserved.

Original languageEnglish
Pages (from-to)205-212
Number of pages8
JournalEuropean Journal of Pharmacology
Volume494
Issue number2-3
Publication statusPublished - 28-Jun-2004

    Keywords

  • MonoHER, reperfusion, oxidative stress, necrosis, neutrophil, cardiac function, DOXORUBICIN-INDUCED CARDIOTOXICITY, MYOCARDIAL-ISCHEMIA, OXIDATIVE STRESS, INFARCT SIZE, INJURY, NEUTROPHIL, MOUSE, HEART, MICE, MONOHYDROXYETHYLRUTOSIDE

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