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

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 i...

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Bibliographic Details
Published in:European journal of pharmacology 2004-06, Vol.494 (2), p.205-212
Main Authors: De Celle, Tijl, Heeringa, Peter, Strzelecka, Agnieska E, Bast, Aalt, Smits, Jos F, Janssen, Ben J
Format: Article
Language:English
Subjects:
Animals
Blood Pressure - drug effects
Cardiac function
Cardiotonic Agents - pharmacology
Dobutamine - pharmacology
Dose-Response Relationship, Drug
Guinea Pigs
Heart Rate - drug effects
Hydroxyethylrutoside - pharmacology
Immunohistochemistry
Male
Mice
MonoHER
Myocardial Contraction - drug effects
Myocardial Infarction - pathology
Myocardial Reperfusion Injury - pathology
Myocardial Reperfusion Injury - physiopathology
Myocardial Reperfusion Injury - prevention & control
Necrosis
Neutrophil
Neutrophil Infiltration - drug effects
Organ Size - drug effects
Oxidative stress
Reperfusion
Ventricular Function - drug effects
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Summary: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.
ISSN:0014-2999
1879-0712
DOI:10.1016/j.ejphar.2004.05.017