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绿茶提取物在大鼠区域性心肌缺血再灌注前给予,通过减轻钙超载来改善心肌收缩力。

Green tea extract given before regional myocardial ischemia-reperfusion in rats improves myocardial contractility by attenuating calcium overload.

机构信息

Department of Life Sciences, National Chung-Hsing University, Taichung 402, Taiwan.

出版信息

Pflugers Arch. 2010 Nov;460(6):1003-14. doi: 10.1007/s00424-010-0881-6. Epub 2010 Oct 5.

Abstract

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.

摘要

有证据表明,绿茶的摄入与心血管疾病呈负相关。本研究旨在探讨在局部心肌缺血前给予绿茶提取物(GTE)是否可以通过防止细胞质 Ca(2+)超载来改善心肌收缩力的抑制。通过结扎左前降支 20 分钟诱导大鼠局部缺血-再灌注(IR),然后松开结扎。没有 GTE 预处理的大鼠在结扎时会引起心室性心律失常,但在 GTE(400mg/kg)预处理 30 分钟后,心律失常的发生减少。在再灌注期间,心律失常仅在最初 5 分钟发生,而 GTE 预处理没有影响。过夜恢复后,对照组再灌注后大鼠的血清 cTnI 水平显著升高,但 GTE 预处理组大鼠的血清 cTnI 水平仅略有升高。在对照组再灌注后大鼠中,超声心动图测量的心肌收缩力在 3 天后仍受到抑制,但在 GTE 预处理组大鼠中则没有。无论是否给予 GTE 预处理,再灌注后的大鼠均未出现心肌缺血损伤。使用新鲜分离的单个心脏肌细胞,发现 GTE 可减轻与再灌注后损伤相关的细胞质 Ca(2+)超载,并调节肌丝、黏附连接和缝隙连接蛋白水平和分布的变化。总之,GTE 预处理通过防止细胞质 Ca(2+)超载、肌丝破坏以及黏附连接和缝隙连接蛋白表达和分布的改变,保护心肌细胞免受 IR 损伤。

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