茶多酚改善大鼠缺血/再灌注心脏功能和能量代谢并抑制体外培养心肌细胞的钙内流（英文）

Tea polyphenols promote cardiac function and energy metabolism in ex vivo rat heart with ischemic/reperfusion injury and inhibit calcium inward current in cultured rat cardiac myocytes

目的探讨茶多酚对缺血/再灌注心脏损伤的保护作用,并研究心脏能量代谢和心肌细胞钙内流是否参与了心脏缺血/再灌注损伤的保护作用。方法在大鼠Langendorff离体心脏上实施缺血/再灌注各30 min,用一导管经压力换能器连接放大器记录心功能指标;用31P NMR技术测定心脏的能量代谢,全细胞膜片钳技术记录心肌细胞钙内流。结果与对照组比较,茶多酚(2.5 mg/L)能使缺血/再灌注心脏的心室发展压、左心室压最大收缩速率(+dp/dt_(max))、左心室压最大舒张速率(-dp/dt_(max))和冠脉流量显著增加(P<0.05),并显著改善缺血/再灌注心脏的能量代谢,增加心肌ATP和PCr含量(P<0.05)。浓度为2.5和5.0 mg/L的茶多酚均能显著抑制培养心肌细胞的钙内流(P<0.01)。结论茶多酚对大鼠离体心脏缺血/再灌注损伤的保护作用可能与其改善心肌能量代谢、抑制心肌细胞钙内流的作用有关。

Objective To investigate the protective effects of tea polyphenols （TP） against myocardial ischemia/reperfusion （IR） injuries and explore the possible mechanisms. Methods Langendorff-perfused rat hearts were subjected to ischemia for 30 min followed by reperfusion for another 30 min. Myocardial function indices were measured by a left ventricular cannula via a pressure transducer connected to the polygraph in isolated Langendorff hearts and energy metabolism was measured using 31P nuclear magnetic resonance （NMR） spectroscopy. Whole-cell patch-clamp technique was used to record calcium inward current （ICa- L） in cultured rat cardiac myocytes. Results Compared with the control hearts, the ex vivo rat hearts with 2.5 mg/L TP treatment showed significantly increased left ventricular developed pressure （LVDP）, maximal rise rate of LVDP （＋dp/dtmax）, maximal fall rate of LVDP （-dp/dtmax）, and coronary flow （CF） （P〈0.05）. During both cardiac ischemia and reperfusion phase, ATP and PCr levels were elevated significantly in TP-treated hearts compared with those in the control hearts （P〈0.05）. In cultured rat cardiac myocytes, ICa-L was remarkably decreased by TP at the doses of 2.5 and 5.0 mg/L （P〈0.01）. Conclusion Our results support a possible protective role of TP against myocardial IR injury by improving myocardial energy metabolism and inhibiting ICa-L in the cardiac myocytes.