蜕皮甾酮对冠状动脉闭塞致大鼠心肌梗死的有益作用及机制  

Beneficial effect of ecdysterone on rat myocardial infarction induced by coronary occlusion

作　　者：吴旭[1] 晋军[2] 梁自文[3] 石富胜[4] 

机构地区：[1]第三军医大学附属大坪医院野战外科研究所,重庆400042 [2]第三军医大学附属新桥医院心内科,重庆400039 [3]第三军医大学附属西南医院内分泌科,重庆400038 [4]中国人民解放军322医院烧伤科,山西大同037006

出　　处：《中草药》2001年第8期721-723,共3页Chinese Traditional and Herbal Drugs

摘　　要：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 ,ip EDS,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 (L DH)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 ,5 0 mg/ kg EDS能剂量依赖地影响大鼠血清 CPK、GOT、L DH活性 ,以 5 mg/ kg剂量的 EDS降低心肌酶谱为最佳。5 m g/ kg EDS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。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 phosphokinase (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 Results 0 5, 5, and 50 mg/kg of phytoecdysone were able to effect the activities of serum CPK, GOT, LDH in a dose depending manner with an optimal effect for improving cardiac zymogram at the dose of 5 mg/kg ip At this dosage EDS can markedly 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

关 键 词：蜕皮甾酮 心肌梗死 冠状动脉闭塞 血管内皮生长因子 

分 类 号：R543.31[医药卫生—心血管疾病] R542.22[医药卫生—内科学]