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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30 min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/dt_(max));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0 min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/dt_(max)[(2327.1±334.5)vs.(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)vs.(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 vs.6.33±1.88,P<0.05);③可明显降低LDH和CK的水平[(282.2±29.6)vs.(222.9±30.2)U/L和(299.8±45.4)vs(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 vs.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。
Objective: To observe the antagonistic effect of traditional Chinese medicine “GXKL” on I / R injury induced by myocardial ischemia / reperfusion (I / R) injury and its possible mechanism. Methods: Thirty-six SD rats were randomly divided into three groups: control group, I / R group and GXKL group, with 12 rats in each group. The I / R model of isolated rat hearts was prepared at 30 min after reperfusion, and the indexes of ex vivo cardiac function were measured: LVDP, HR, LVEDP and ventricular (± dp / dt max); (2) Arrhythmia score; (3) Biochemical tests were used to detect the activity of creatine kinase (CK) and lactate dehydrogenase (LDH); min, the level of JNK phosphorylation in myocardial tissue. RESULTS: Compared with I / R group, GXKL group: ① significantly increased ± dp / dt max in myocardium of I / R rats [(2327.1 ± 334.5) vs. (1823.1 ± 499.8) mmHg / s, P < (P <0.05). LVEDP: (19.9 ± 9.9) vs. (31.0 ± 9.4) mmHg, P <0.05), and significantly improved the indexes of LVDP and LVEDP [LVDP: 39.6 ± 9.1 vs. 24.2 ± 10.1 mmHg, 0.05] .②The level of LDH and CK was significantly lower than that of the control group (P <0.05); ② The level of arrhythmia was significantly lower (11.58 ± 4.81 vs.6.33 ± 1.88, P <0.05) L and (299.8 ± 45.4) vs (251.9 ± 41.8) U / L, P <0.05]; ④The level of phosphorylated JNK in ischemic myocardium was significantly decreased (0.75 ± 0.07 vs.1.54 ± 0.10, P <0.05) . Conclusion: GXKL can significantly improve the ability of ischemia-reperfusion myocardium against ischemia and hypoxia, increase myocardial contractility and reduce arrhythmia. Its antagonism to I / R of isolated myocardium may be closely related to JNK pathway.