“冠心颗粒”抗缺血／再灌注损伤作用及JNK蛋白信号通路在其中的调节作用

目的：观察具有抗心肌缺血／再灌注（I／R）损伤作用的中药“冠心颗粒”（GXKL）对心肌I／R损伤的拮抗作用及其可能的机制。方法：将36只SD大鼠随机分为3组：对照组，I／R组及GXKL组，每组12只大鼠。制备大鼠离体心脏心肌I／R模型再灌注30rain时，分别检测①离体心脏功能指标：左室收缩压（LVDP）、心率（HR）、左室舒张末压（LVEDP）及心室内压最大变化率（±dp／dtmax）；②心律失常评分；③应用生化法检测肌酸激酶（CK）和乳酸脱氢酶（LDH）的活性；④应用蛋白印迹法检测再灌注0min时，心肌组织中JNK的磷酸化水平。结果：与I／R组比较，GXKL组：①可明显提高I／R大鼠心肌中的±dp／dtmax（2327．1±334．5）US．（1823．1±499．8）mmHg／s，P〈0．05]，并明显改善LVDP、LVEDP等指标LVDP：（39．6±9．1）vs．（24．2±10．1）mmHg，P〈0．05；LVEDP：（19．9±9．9）摊．（31．0±9．4）mmHg，P〈0．05]；②可明显降低心律失常的评分（11．58±4．81郴．6．33±1．88，P〈0．05）；③可明显降低LDH和CK的水平（282．2±29．6）YS．（222．9±30．2）U／L和（299．8±45．4）US．（251．9±41．8）U／L，P〈0．05]；④可明显降低缺血心肌组织中磷酸化JNK的水平（0．75±0．07椰．1．54±0．10，P〈0．05）。结论：GXKL可明显改善缺血心肌抗缺血、缺氧的能力，增加心肌收缩力，减轻心律失常；其对离体心肌I／R的拮抗作用可能与JNK途径密切相关。

Guanxinkeli protects myocardial cell from ischemia-reperfusion injury in rats via JNK signal pathway

AIM ： To study the protection due to guanxinkeli （GXKL） on myocardial ischemic and reperfusion injury. METHODS： Thirty six rats were randomly divided into three groups： control, ischemia reperfusion injury, and resveratrol. Rat hearts were subjected to 15 rain ischemia and then followed by 30 min reperfusion. HR, LVDP, LVEDP and -＋ dp/dtmax were recorded before ischemia and at 30 min of reperfusion. Coronary effulent was collected before ischemia and at 30 min of reperfusion to measure the CK and LDH activity. The arrhythmia scores were determined. RESULTS： GXKL enhanced the LVEDP, LVDP and _＋ dp/dtmaX. The arrhythmia score, CK and LDH activity were lower in the GXKL group than in ischemia and reperfusion group. JNK activity was also lower in the GXKL group. CONCLUSION： GXKL has protected isolated myocardial ischemia and reperfusion injury. The JNK signaling pathway may play an important role in the mechanism.