中文摘要：

目的：观察竹节参总皂苷对大鼠心肌梗死的保护作用,并初步探讨其发挥作用的机制。方法：通过结扎左冠状动脉前降支建立大鼠心肌梗死模型,模型成功后随机分为模型组、竹节参总皂苷组（50 mg/kg、100 mg/kg）,连续灌胃给药4周,假手术组和模型组给予等体积的生理盐水。4周后进行心功能检测;取心脏,称重后计算心脏重量指数;HE、Masson、苦味酸-天狼星红染色,观察心肌组织形态并计算胶原容积分数。取血清,检测SOD、CAT、GSH-Px的活性和MDA的含量;ELISA法检测TNF-α、TGFβ炎症因子的含量。结果：模型组大鼠心功能明显受损,心脏重量指数升高,并发生纤维化;血清中抗氧化物酶的活性降低,脂质过氧化物含量升高,且炎症因子含量升高,与假手术组比较有显著性差异。竹节参总皂苷（50 mg/kg、100 mg/kg）能使以上症状得到显著改善。结论：竹节参总皂苷对心肌梗死大鼠具有保护作用,其作用机制可能与降低氧化应激反应和炎症损伤相关。

英文摘要：

Objective：To observe the cardioprotective effects of saponins from Panax japonicus（SPJ） on myocardial infarction in rats and the possible mechanism of it.Methods： Myocardial infarction injury rats induced by ligating of the left anterior descending branch（LAD）,rats were randomly divided into four groups： sham-operated,LAD,LAD ＋ SPJ（SPJ,50mg/kg/day and 100mg/kg/day,orally）.After operation the foregoing groups were pretreated with homologous drug once a day for 4 weeks respectively;sham-operated and LAD were given an equal volume of saline.Four weeks later,we evaluate cardiac function;and hearts were harvested to assess heart weight index;histopathological damages and Collagen volume fraction were evaluated by He,Masson,and picric acid-Sirius red staining.Blood samples were collected to determine serum levels of superoxide dismutase（SOD）,catalase（CAT）,glutathione peroxidase（GSH-Px）,malondialdehyde（MDA）;inflammatory factors TNF-α and TGFβ were Detected by ELISA.Results： Myocardial infarction induced by ligation of LAD significantly suppressed cardiac function,increased heart weight index and fibrosis;we also found a significant increase in oxidative stress as evidenced by increases in the downregulation of SOD,CAT,GSH-Px and upregulation of MAD.In parallel there was a significant increase in inflammatory cytokine levels,such as TNF-α and TGFβ.It showed significant difference between sham group and LAD group.SPJ（50 mg/kg and 100 mg/kg） can significantly improve these symptoms.Conclusion： The results suggest that SPJ plays a protective role on myocardial infarction in rats,and the possibility of its mechanism may reduce oxidation stress and inflammatory response.