摘要
目的探讨葛根素对慢性缺氧小鼠心肌的保护作用。方法建立小鼠慢性缺氧模型30只,随机分为葛根素治疗组、缺氧组各15只,另设正常对照组10只。实验2周后处死小鼠,取新鲜心肌标本,检测琥珀酸脱氢酶(SDH)、三磷酸腺苷酶(ATP)、乳酸脱氢酶(LDH),并进行光镜、电镜下心肌病理形态及超微结构变化的比较观察。结果缺氧组SDH、ATP降低,LDH升高,心肌间质水肿,心肌细胞线粒体肿胀,肌丝排列紊乱,与对照组及葛根素治疗组比较有显著差异(P<0.01);葛根素治疗组心肌酶和心肌超微结构与对照组相比均无显著差异(P>0.05)。结论慢性缺氧可以导致心肌酶和心肌超微结构的改变;缺氧导致心肌损伤后心肌酶改变比超微结构改变更敏感;葛根素具有保护心肌、改善心功能的作用。
Objective To investigate the protective effect of puerarin on myocardiumin of anoxia-mice. Methods： 40 chronic hypoxia mice models wers established and derided randomly into 3 groupsz puerarin group, anoxia group and the control group. All the mice were killed after two weeks, the myocardium samples were taken immediately. Myocardium succinic dehyrogenase （SDH）, adenosine trphosphatase （ATP）, lactic dehydrogenase （LDH） were measured. Pathologic and ultrastructure changes of myocardium were observed under the light and electric microscopes. Results, SDH and ATP decrease in hypoxia mice and LDH increase were observed; in addition, the mesenchyma was edematous and mitochondrions of myocardial were enlarged; the arragement of filaments was irregular. Compared with puerarin and control groups, the difference was significanct （P〈0. 01）. However, there was no significant difference in puerarin and control groups （P〉0. 05）. Conclusion： 1. Chronic anoxia can cause harm of myocardial and mitoehondrions in myocardial, the former is more sesitive than the latter. 2. The hypoxia can protect myocardium and improve the function Of the heart.
出处
《山东医药》
CAS
北大核心
2006年第5期15-16,共2页
Shandong Medical Journal
基金
山东省卫生厅基金项目(2001CA1CCB7)
关键词
葛根素
缺氧
心肌损伤
心肌保护
puerarin
anoxia
myocardial jnjury
myocardial protects
