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2.
Life Sci ; 79(3): 217-24, 2006 Jun 13.
Article in English | MEDLINE | ID: mdl-16458326

ABSTRACT

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.


Subject(s)
Cardiotonic Agents/pharmacology , Heart/drug effects , Isoflavones/pharmacology , Mitochondrial Membrane Transport Proteins/metabolism , Myocardial Reperfusion Injury/prevention & control , Potassium Channels/metabolism , Animals , Atractyloside/pharmacology , Cardiotonic Agents/antagonists & inhibitors , Decanoic Acids/pharmacology , Hydroxy Acids/pharmacology , In Vitro Techniques , Isoflavones/antagonists & inhibitors , Male , Mitochondrial Permeability Transition Pore , Myocardial Reperfusion Injury/metabolism , Myocardium/metabolism , Potassium Channel Blockers/pharmacology , Potassium Channels/drug effects , Rats , Rats, Sprague-Dawley
3.
Article in Chinese | MEDLINE | ID: mdl-21155274

ABSTRACT

AIM: To determine whether the cardioprotection of puerarin (Pue) against ischemia/reperfusion (I/R) is mediated by mitochondrial transmembrane pore or channels. METHODS: Male Sprague-Dawley rats were used for Langendorff isolated heart perfusion. The hearts subjected to global ischemia for 30 min followed by 120 min of reperfusion. Formazan, a product of 2,3,5-triphenyltetrazolium chloride (TTC), which is proportional to myocardial viability, was measured at 490 nm, and the level of lactate dehydrogenase (LDH) in the coronary effluent was measured to evaluate the cardiac injury. RESULTS: The pretreatment with Pue at 0.24 mmol/L for 5 min before ischemia increased formazan content of myocardium, reduced LDH release, improved the recovery of the left ventricular developed pressure, maximal rise/fall rate of left ventricular pressure, left ventricular end-diastolic pressure and rate pressure product (left ventricular developed pressure multiplied by heart rate) and attenuated the decrease of coronary flow during reperfusion. Administration of atractyloside (20 micromol/L), an opener of mitochondrial permeability transition pore, for 20 min (first 20 min of reperfusion) and 5-hydroxydecanoate (100 micromol/L), the mitochondrial specific K(ATP) blocker, for 20 min before ischemia attenuated the protective effects of Pue. CONCLUSION: The findings indicate that in the isolated rat heart, Pue protects myocardium against ischemia/ reperfusion injury via the opening of mitochondrial ATP-sensitive potassium channel and the inhibition of mitochondrial permeability transition pore opening.


Subject(s)
Isoflavones/pharmacology , Mitochondria, Heart/drug effects , Mitochondrial Membrane Transport Proteins/drug effects , Myocardial Reperfusion Injury/metabolism , Animals , Decanoic Acids/metabolism , Hydroxy Acids/metabolism , Male , Mitochondria, Heart/metabolism , Mitochondrial Permeability Transition Pore , Rats , Rats, Sprague-Dawley
4.
Conf Proc IEEE Eng Med Biol Soc ; 2005: 5591-4, 2005.
Article in English | MEDLINE | ID: mdl-17281523

ABSTRACT

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. In isolated rat hearts subjected to 30 min regional ischemia and 120 min reperfusion, pretreatment with Pue at 0.24 mmol/L for 5 min before ischemia increased myocardial formazan content, an index of myocardial viability, reduced lactate dehydrogenase release, improved recovery of the maximal rise/fall rate of left ventricular pressure, 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 Ca2+-induced swelling was observed, and this inhibition was attenuated by 5-hydroxydecanoate. These findings indicate that Pue 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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