Abstract
Curcumin is an inhibitor of p300 histone acetyltransferase activity, which is associated with the deterioration of heart failure. We reported that native curcumin, at a dosage of 50 mg/kg, prevented deterioration of the systolic function in rat models of heart failure. To achieve more efficient oral pharmacological therapy against heart failure by curcumin, we have developed a novel drug delivery system (DDS) which markedly increases plasma curcumin levels. At the dosage of 0.5 mg/kg, DDS curcumin but not native curcumin restored left ventricular fractional shortening in post-myocardial infarction rats. Thus, our DDS strategy will be applicable to the clinical setting in humans.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Administration, Oral
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Animals
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Cardiotonic Agents / administration & dosage*
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Cardiotonic Agents / pharmacokinetics
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Curcumin / administration & dosage*
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Curcumin / pharmacokinetics
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Disease Models, Animal
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Drug Delivery Systems
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Gum Arabic / administration & dosage
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Heart Failure / drug therapy*
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Heart Failure / pathology
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Heart Failure / physiopathology
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Hemodynamics
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Intestinal Absorption / drug effects
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Male
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Myocardial Infarction / drug therapy*
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Myocardial Infarction / pathology
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Myocardial Infarction / physiopathology
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Plant Gums / administration & dosage*
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Rats
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Rats, Sprague-Dawley
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p300-CBP Transcription Factors / antagonists & inhibitors
Substances
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Cardiotonic Agents
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Plant Gums
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Gum Arabic
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p300-CBP Transcription Factors
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p300-CBP-associated factor
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Curcumin
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gum ghatti