Document Detail


Atractyloside and 5-hydroxydecanoate block the protective effect of puerarin in isolated rat heart.
MedLine Citation:
PMID:  16458326     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Qin Gao; Hong-Yang Pan; Shuang Qiu; Yuan Lu; Iain C Bruce; Jian-Hong Luo; Qiang Xia
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Publication Detail:
Type:  In Vitro; Journal Article     Date:  2006-02-02
Journal Detail:
Title:  Life sciences     Volume:  79     ISSN:  0024-3205     ISO Abbreviation:  Life Sci.     Publication Date:  2006 Jun 
Date Detail:
Created Date:  2006-06-01     Completed Date:  2006-08-04     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0375521     Medline TA:  Life Sci     Country:  England    
Other Details:
Languages:  eng     Pagination:  217-24     Citation Subset:  IM    
Affiliation:
Department of Physiology, Zhejiang University School of Medicine, 353 Yan-an Road, Hangzhou 310031, China.
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MeSH Terms
Descriptor/Qualifier:
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:
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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