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目的:观察芍药苷对大鼠心肌缺血再灌注(myocardial ischemia/reperfusion,MI/R)损伤的保护作用,探讨其作用机制。方法:结扎冠脉造成心肌缺血30 min再灌注2 h,建立MI/R损伤大鼠模型,随机分为假手术组、模型组、芍药苷三个剂量组(20,10,5 mg·kg-1)(n=10),于术前1 h和再灌注即刻分别进行尾静脉注射给药。取血清,测定肌酸激酶(CK)、乳酸脱氯酶(LDH)、超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量;取心脏,测定心肌梗死面积。结果:芍药苷高、中剂量可明显缩小大鼠心肌梗死面积,与模型组比较差异有统计学意义(P<0.05);芍药苷各剂量组可不同程度降低血清CK和LDH活性(P<0.05或P<0.01),升高SOD活性(P<0.01);芍药苷高、中剂量组降低血清MDA含量,与模型组比较差异有统计学意义(P<0.05)。结论:芍药苷预处理对MI/R损伤的保护作用与其减少自由基的生成、抑制脂质过氧化反应等有关。
Objective: To observe the protective effect of paeoniflorin on myocardial ischemia / reperfusion (MI / R) injury in rats and its mechanism. Methods: Myocardial ischemia was induced by ligating the coronary artery for 30 min and then reperfused for 2 h. Mice with MI / R injury were established and randomly divided into sham operation group, model group and paeoniflorin (20, 10, and 5 mg · kg -1) -1) (n = 10). The animals were injected intravenously 1 h before and immediately after reperfusion, respectively. The serum was taken and the activity of creatine kinase (CK), lactate dehydrogenase (LDH) and superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were measured. Results: Paeoniflorin at high dose and medium dose significantly reduced the area of myocardial infarction in rats, which was significantly different from that of model group (P <0.05). Paeoniflorin could decrease the activities of serum CK and LDH (P <0.05) (P <0.01 or P <0.01), and increased SOD activity (P <0.01). Paeoniflorin high and medium dose groups decreased serum MDA content, which had statistical significance compared with model group (P <0.05). Conclusion: The protective effect of paeoniflorin on MI / R injury is related to reducing the production of free radicals and inhibiting lipid peroxidation.