Abstract
Myocardial ischemia and reperfusion (MI/R) is associated with an intense inflammatory reaction, which may lead to myocyte injury. In this study, we investigated the effect of quercetin, an inhibitor of c-Jun N-terminal kinase on ischemia/reperfusion injury in isolated rat hearts. Rat models of MI/R were induced by coronary occlusion followed by reperfusion, treatment of rats with quercetin (1.0 mg/kg, i.v.) induced a significant reduction of infarct volume and improvements in baseline hemodynamic abnormalities (P < 0.05). Quercetin treatment also attenuated the expression of both TNF-alpha (TNF-α) and interleukin-10 (IL-10) and lowered the serum levels of inflammatory cytokine (P < 0.05). These findings suggested that quercetin treatment significantly attenuated MI/R injury primarily through anti-inflammatory effects.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Gene Expression Regulation / drug effects
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Hemodynamics / drug effects
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Interleukin-10 / metabolism
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Male
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Myocardial Infarction / drug therapy
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Myocardial Infarction / genetics
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Myocardial Infarction / pathology
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Myocardial Infarction / physiopathology
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Myocardial Reperfusion Injury / drug therapy*
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Myocardial Reperfusion Injury / genetics
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Myocardial Reperfusion Injury / physiopathology
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Myocardium / metabolism
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Myocardium / pathology
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Protective Agents / pharmacology
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Protective Agents / therapeutic use*
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Quercetin / pharmacology
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Quercetin / therapeutic use*
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Rats
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Rats, Sprague-Dawley
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Tumor Necrosis Factor-alpha / genetics
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Tumor Necrosis Factor-alpha / metabolism
Substances
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Protective Agents
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RNA, Messenger
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Tumor Necrosis Factor-alpha
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Interleukin-10
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Quercetin