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|標題:||Green tea extract given before regional myocardial ischemia-reperfusion in rats improves myocardial contractility by attenuating calcium overload||作者:||Liou, Y.M.
|關鍵字:||Green tea extract (GTE);Ca(2+) overload;Ischemia-reperfusion (IR);Adhesion molecules;Arrhythmia;Gap junctions;isolated rabbit hearts;ventricular-fibrillation;gap-junctions;injury;polyphenol;mechanisms;cardioprotection;redistribution;infarction;connexin43||Project:||Pflugers Archiv-European Journal of Physiology||期刊/報告no：:||Pflugers Archiv-European Journal of Physiology, Volume 460, Issue 6, Page(s) 1003-1014.||摘要:||
There is evidence for a negative correlation between green tea consumption and cardiovascular diseases. The aim of the present study was to examine whether green tea extract (GTE) given before regional myocardial ischemia could improve depression of myocardial contractility by preventing cytosolic Ca(2+) overload. Regional ischemia-reperfusion (IR) was induced in rats by ligating the left anterior descending branch for 20 min, then releasing the ligature. Ligation induced ventricular arrhythmias in rats without GTE pretreatment, but decreased arrhythmogenesis was seen in rats pretreated 30 min earlier with GTE (400 mg/kg). During reperfusion, arrhythmias only occurred during the initial 5 min, and GTE pretreatment had no effect. After overnight recovery, serum cTnI levels were greatly increased in control post-IR rats but only slightly elevated in GTE-pretreated post-IR rats. Myocardial contractility measured by echocardiography was still depressed after 3 days in control post-IR rats, but not in GTE-pretreated post-IR rats. No myocardial ischemic injury was seen in post-IR rats with or without GTE pretreatment. Using freshly isolated single heart myocytes, GTE was found to attenuate the post-IR injury-associated cytosolic Ca(2+) overload and modulate changes in the levels and distribution of myofibril, adherens junction, and gap junction proteins. In summary, GTE pretreatment protects cardiomyocytes from IR injury by preventing cytosolic Ca(2+) overload, myofibril disruption, and alterations in adherens and gap junction protein expression and distribution.
|Appears in Collections:||生命科學系所|
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