京尼平苷对大鼠心肌缺血再灌注损伤的保护作用

Protective effects of geniposide on ischemia-reperfusion injury in rats

【目的】研究京尼平苷(Geniposide,Gen)对大鼠心肌缺血再灌注损伤的保护作用及其机制。【方法】采用开胸结扎冠状动脉左降支的方法,制备大鼠心肌缺血再灌注模型。40只大鼠随机分成5组:假手术组、缺血再灌注模型组、京尼平苷低剂量组、京尼平苷中剂量组、京尼平苷高剂量组,每组各8只。连续监测Ⅱ导心电图(ECG),比色法检测血清中肌酸激酶(CK)、乳酸脱氢酶(LDH)含量,硫代巴比妥酸法测定心肌组织中丙二醛(MDA)含量,黄嘌呤氧化酶法测定心肌组织中超氧化物歧化酶(SOD)活力。【结果】与模型组相比,京尼平苷低、中、高3个剂量组显著降低ST-段抬高幅度(P<0.01)、CK值(P<0.01)、LDH值(P<0.05)、MDA值(P<0.05),SOD值明显增高(P<0.05)。【结论】京尼平苷能够明显减轻缺血再灌注对心肌细胞损伤程度,对心肌有明显的保护作用,其机制可能与其能够提高SOD活力、减少MDA生成有关。

[Objective]To investigate the effect of geniposide（Gen）on myocardial ischemia-reperfusion injury in rats.[Methods]Myocardial ischemia/reperfusion injury model of rats were made by opening the chest and ligating the left anterior descending coronary artery（LAD）.40 rats were divided randomly into 5 groups：Sham group,Model group,Gen low dose group,Gen meddle dose group,Gen high dose group.The changes of ST segment were measured.The content of the serum creatine phosphokinase（CK）,lactate dehydrogenase（LDH）and the myocardial malondialdehyde（MDA）were examined.The activity of myocardial superoside dismutase（SOD）was determined.[Results]Compared with model group,the elevation of ST segment,the content of the serum CK and LDH were significantly decreased（P〈0.05）by Gen groups.The activity of myocardial SOD was significantly increased（P〈0.05）and the content of myocardial MDA was significantly decreased（P〈0.05）by Gen groups.[Conclusion] Myocardial of rats were protected by Gen from ischemia/reperfusion injury by decreasing of the content of MDA,increasing of the activity of SOD.