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目的探讨黄精多糖(PSP)对急性心肌梗死模型(AMI)大鼠损伤的保护作用及可能机制。方法采用结扎冠状动脉左前降支的方法制备心肌梗死动物模型,假手术组只穿线不结扎,将造模成功的大鼠随机分为模型组、黄精多糖高、中、低剂量组(900 mg/kg、450 mg/kg、225 mg/kg)及阳性组(麝香保心丸,12.2 mg/kg·d),每组10只,每日灌胃1次,连续4周。分别记录造模前、造模即刻及给药1、3、7、10、14、21、28 d心电图S-T段变化,采用酶联免疫吸附法(ELISA)测定各组大鼠血清中肿瘤坏死因子α(TNF-α)、白介素6(IL-6)、谷胱甘肽过氧化物酶(GSH-Px)及丙二醛(MDA)含量;显微镜下观察受损心肌病理学的改变。结果与模型组相比,黄精多糖能明显抑制心肌梗死模型大鼠S-T段的升高;各给药组大鼠血清IL-6、TNF-α水平均显著降低(P<0.05或0.01),GSH-Px活性升高(P<0.05或0.01),并降低MDA含量(P<0.05或0.01),心肌损伤程度明显改善。结论 PSP对急性心肌梗死模型大鼠心肌损伤有保护作用,其作用机制可能与减轻炎症反应,提高氧自由基清除能力,减少脂质过氧化损伤有关。
Objective To investigate the protective effect of Polygonatum Polysaccharide (PSP) on the injury of acute myocardial infarction (AMI) rats and its possible mechanism. Methods The animal model of myocardial infarction was established by ligation of the left anterior descending artery of coronary artery. The rats in the sham operation group were not ligated by threading. The successful rats were randomly divided into model group, high, medium and low doses of Polygonatum Polysaccharide (900 mg / kg, 450 mg / kg, 225 mg / kg) and positive group (12.2 mg / kg · d). Each group was given gavage once a day for 4 weeks. The changes of ST segment of electrocardiogram were recorded before modeling, immediately after modeling and on the 1st, 3rd, 7th, 10th, 14th, 21st, 28th day after administration. The levels of tumor necrosis factor α, TNF-α, IL-6, GSH-Px and MDA were measured. The pathological changes of injured myocardium were observed under microscope. Results Compared with the model group, Polygonatum Polysaccharides could significantly inhibit ST-segment elevation in rats with myocardial infarction. The levels of IL-6 and TNF-α in serum of rats in each group were significantly decreased (P <0.05 or 0.01) -Px activity (P <0.05 or 0.01), and decreased MDA content (P <0.05 or 0.01), myocardial injury significantly improved. Conclusion PSP has a protective effect on myocardial injury in acute myocardial infarction model rats. Its mechanism may be related to the reduction of inflammatory reaction, the improvement of oxygen free radical scavenging ability and the reduction of lipid peroxidation injury.