Abstract
Acute myocardial infarction (AMI) is associated with inflammation and apoptosis. Emodin plays an anti-inflammatory role in several inflammatory diseases. Recent studies have demonstrated that emodin protects against myocardial ischemia/reperfusion injury. However, its mechanism underlying its effects remains unknown. In a murine model of AMI, based on ligation of the left coronary artery, administration of emodin reduced myocardial infarct size (MIS) in a dose-dependent manner. Emodin significantly suppressed TNF-alpha expression and NF-kappaB activation in the local myocardial infarction area. Treatment with emodin inhibited myocardial cell apoptosis by inhibiting caspase-3 activation. Therefore, these studies demonstrate that emodin protects against myocardial cell injury via suppression of local inflammation and apoptosis.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
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Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
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Apoptosis / drug effects*
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Blotting, Western
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Disease Models, Animal
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Electrophoretic Mobility Shift Assay
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Emodin / pharmacology*
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Emodin / therapeutic use
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Enzyme-Linked Immunosorbent Assay
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Flow Cytometry
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Male
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Mice
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Mice, Inbred BALB C
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Myocardial Infarction* / immunology
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Myocardial Infarction* / pathology
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Myocardial Infarction* / prevention & control
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Myocardium* / enzymology
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Myocardium* / immunology
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Myocardium* / pathology
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NF-kappa B / metabolism
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Peroxidase / metabolism
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Reverse Transcriptase Polymerase Chain Reaction
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Tumor Necrosis Factor-alpha / antagonists & inhibitors
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Tumor Necrosis Factor-alpha / immunology
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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NF-kappa B
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Tumor Necrosis Factor-alpha
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Peroxidase
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Emodin