南方医科大学学报

南方医科大学学报 ›› 2016, Vol. 36 ›› Issue (05): 604-.

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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

DONG Huajin1, LI Jie2, ZHAN Hao3, LI Yang2, SU Ruibin1   

  1. 1State Key Laboratory of Toxicology and Medical Countermeasures, Beijing Key Laboratory of Neuropsychopharmacology, Beijing Institute of Pharmacology and Toxicology, Beijing 100039, China; 2General Hospital of PLA, Beijing 100853, China; 3Institute of Aviation Medicine, Beijing 100142, China
  • 出版日期:2016-05-20 发布日期:2016-05-20

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

董华进，李捷，詹皓，李泱，苏瑞斌   

  1. 1State Key Laboratory of Toxicology and Medical Countermeasures, Beijing Key Laboratory of Neuropsychopharmacology, Beijing Institute of Pharmacology and Toxicology, Beijing 100039, China; 2General Hospital of PLA, Beijing 100853, China; 3Institute of Aviation Medicine, Beijing 100142, China
  • Online:2016-05-20 Published:2016-05-20

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摘要： 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/dtmax）、左心室压最大舒张速率（-dp/dtmax）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。

Abstract: 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.