| Atractyloside and 5-hydroxydecanoate block the protective effect of puerarin in isolated rat heart. | |
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MedLine Citation:
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PMID: 16458326 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The aim of the present study was to determine whether the clinically effective cardioprotection conferred by puerarin (Pue) against ischemia and reperfusion is mediated by mitochondrial transmembrane pores and/or channels. Hearts isolated from male Sprague-Dawley rats were perfused on a Langendorff apparatus and subjected to 30 min of global ischemia followed by 120 min of reperfusion. The production of formazan, which provides an index of myocardial viability, was measured by absorbance at 550 nm, and the level of lactate dehydrogenase (LDH) in the coronary effluent was determined. In this model, Pue (0.0024-2.4 mmol/l) had a dose-dependent, negatively inotropic effect. Pretreatment with Pue at 0.24 mmol/l for 5 min before ischemia increased myocardial formazan content, reduced LDH release, improved recovery of left ventricular end-diastolic pressure and rate-pressure product (left ventricular developed pressure multiplied by heart rate) during reperfusion. Administration of atractyloside (20 micromol/l), an opener of the mitochondrial permeability transition pore, for the first 20 min of reperfusion, and 5-hydroxydecanoate (100 micromol/l), the mitochondrial-specific ATP-sensitive potassium channel blocker, for 20 min before ischemia, attenuated the protective effects of Pue. In mitochondria isolated from hearts pretreated with 0.24 mmol/l Pue for 5 min, a significant inhibition of Ca(2+)-induced swelling was observed, and this inhibition was attenuated by 5-hydroxydecanoate. In isolated ventricular myocytes, pretreatment with Pue prevented ischemia-induced cell death and depolarization of the mitochondrial membrane, and atractyloside and 5-hydroxydecanoate attenuated the effects of Pue. These findings indicate that puerarin protects the myocardium against ischemia and reperfusion injury via inhibiting mitochondrial permeability transition pore opening and activating the mitochondrial ATP-sensitive potassium channel. |
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Authors:
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Qin Gao; Hong-Yang Pan; Shuang Qiu; Yuan Lu; Iain C Bruce; Jian-Hong Luo; Qiang Xia |
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Publication Detail:
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Type: In Vitro; Journal Article Date: 2006-02-02 |
Journal Detail:
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Title: Life sciences Volume: 79 ISSN: 0024-3205 ISO Abbreviation: Life Sci. Publication Date: 2006 Jun |
Date Detail:
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Created Date: 2006-06-01 Completed Date: 2006-08-04 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0375521 Medline TA: Life Sci Country: England |
Other Details:
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Languages: eng Pagination: 217-24 Citation Subset: IM |
Affiliation:
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Department of Physiology, Zhejiang University School of Medicine, 353 Yan-an Road, Hangzhou 310031, China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Atractyloside / pharmacology Cardiotonic Agents / antagonists & inhibitors, pharmacology* Decanoic Acids / pharmacology Heart / drug effects* Hydroxy Acids / pharmacology Isoflavones / antagonists & inhibitors, pharmacology* Male Mitochondrial Membrane Transport Proteins / metabolism* Myocardial Reperfusion Injury / metabolism, prevention & control* Myocardium / metabolism Potassium Channel Blockers / pharmacology Potassium Channels / drug effects, metabolism* Rats Rats, Sprague-Dawley |
| Chemical | |
Reg. No./Substance:
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0/Cardiotonic Agents; 0/Decanoic Acids; 0/Hydroxy Acids; 0/Isoflavones; 0/Mitochondrial Membrane Transport Proteins; 0/Potassium Channel Blockers; 0/Potassium Channels; 0/mitochondrial K(ATP) channel; 0/mitochondrial permeability transition pore; 17754-44-8/Atractyloside; 3681-99-0/puerarin; 624-00-0/5-hydroxydecanoic acid |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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