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目的 探讨植物药有效成分蜕皮甾酮 (ecdysterone, EDS)对心肌梗死有益作用, 并探讨其机制。 方法 采用冠状动脉左前降支结扎致大鼠心肌梗死模型, ipEDS, 连续7d。 测定血清肌酸磷酸激酶(CPK)、谷草转氨酶(GOT)、乳酸脱氢酶(LDH)活性、心肌梗死面积、冠状动脉血流量、毛细血管密度及血管内皮生长因子(VEGF)的表达量。 结果 0 .5, 5, 50mg/kgEDS能剂量依赖地影响大鼠血清CPK、GOT、LDH活性, 以5mg/kg剂量的EDS降低心肌酶谱为最佳。 5mg/kgEDS能明显减少心肌梗死面积、增加冠状动脉血流量、毛细血管密度和VEGF表达量。 结论 EDS能减轻冠状动脉结扎致心肌梗死, 机制在于促进VEGF的表达和毛细血管再生及增加冠状动脉血流量。
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[Abstract]
Object To explore the beneficial effect of phytoecdysone(EDS) on myocardial infarction and its mechanism of action. Methods Rat myocardial infarction model was prepared by ligating the left anterior descending coronary artery, and EDS was injected ip for seven consecutive days. Serum creatine phosphoki nase(CPK) glutamic-oxalacetic transaminase(GOT), lactic dehydrogenase(LDH) activities, infarct size(IS), coronary blood flow, capillary vessel density and vascular endothelial growth factor(VEGF) expression were determined. b>Results 0.5, 5, and 50mg/kg of phytoecdysone were able to ef-fect the activities of serum CPK, GO T, LDH in a dose depending manner with an optimal effect for im-proving cardiac zymogram at the dose of 5mg/kg ip. At this dosage EDS canmarkedly reduce IS, increase coronary blood flow, capillary vessel density and the expression of VEGF. Conclusion ESD can alleviate myocardial infarction symptoms. The mechanism of such beneficial effect may due to its ability to promote VEGF expression regeneration of capillary vessels and increase coronary blood flow.
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