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

被引：28

作者：

De Celle, T ^{[1
]}

Heeringa, P ^{[1
]}

Strzelecka, AE ^{[1
]}

Bast, A ^{[1
]}

Smits, JF ^{[1
]}

Janssen, BJ ^{[1
]}

机构：

[1] Univ Maastricht, Cardiovasc Res Inst Maastricht, Dept Pharmacol & Toxicol, Maastricht, Netherlands

来源：

EUROPEAN JOURNAL OF PHARMACOLOGY | 2004年 / 494卷 / 2-3期

关键词：

MonoHER; reperfusion; oxidative stress; necrosis; neutrophil; cardiac function;

D O I：

10.1016/j.ejphar.2004.05.017

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

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.

引用

页码：205 / 212

页数：8

共 29 条

[1] The new cardioprotector Monohydroxyethylrutoside protects against doxorubicin-induced inflammatory effects in vitro [J].