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机构地区:[1]北京中医药大学中药药理系,北京100102 [2]苏州玉森新药开发有限公司,苏州215125
出 处:《中药药理与临床》2010年第5期45-47,共3页Pharmacology and Clinics of Chinese Materia Medica
摘 要:目的:探讨梓醇对脑缺血大鼠恢复早期脑能量代谢的影响。方法:线栓法建立SD大鼠右侧大脑中动脉永久性缺血模型(pMCAO),于术后3d开始给药,术后14d取材,测定各组大鼠脑组织中钠、钾-三磷酸腺苷酶(Na+、K+-ATPase)和钙、镁-三磷酸腺苷酶(Ca2+、Mg2+-ATase)活性。结果:模型组与假手术组比较,Na+、K+-ATPase和Ca2+、Mg2+-ATPase活性明显降低,表明模型组在术后14d未自行恢复到正常水平。模型组与各给药组比较,Na+、K+-ATPase和Ca2+、Mg2+-ATPase活性差异均具有显著意义。结论:梓醇抑制脑缺血大鼠细胞凋亡的机理与Na+、K+-ATPase和Ca2+、Mg2+-ATPase升高有关。Objective:To investigate the effect of catalpol on brain energy metabolism after permanent cerebral ischemia in rats.Method:Permanent cerebral ischemia was induced by permanent middle cerebral artery occlusion(pMCAO) in rats,and ischemic medication animals received intragastric administration once a day 3-14 days post-ischemia.Animals were killed at 14 days post ischemia.The inorganic phosphate assay method were used to evaluate the activity of Na+,K+-ATPase and Ca2+,Mg2+-ATPase of ischemic cortex.Result:There were significant difference of two indexes between sham operation group and model group(P〈0.01).And there were significant difference of two indexs between sham operation group and every treatment group(P〈0.05,P〈0.01).Conclusion:The mechanism of inhibiting apoptosis of rats brain cell from permanent cerebral ischemia by catalpol is well related to the increase of Na+,K+-ATPase and Ca2+,Mg2+-ATPase.
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