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作 者:韩淑燕[1,2] 马旭[1,3] 李海霞[1] 张可[1] 屠鹏飞[1]
机构地区:[1]北京大学药学院天然药物及仿生药物国家重点实验室,北京100191 [2]北京大学临床肿瘤学院北京肿瘤医院暨北京市肿瘤防治研究所恶性肿瘤发病机制及转化研究教育部重点实验室,北京100142 [3]国家知识产权局专利局专利审查协作中心,北京100183
出 处:《中国药理学与毒理学杂志》2012年第4期499-503,共5页Chinese Journal of Pharmacology and Toxicology
基 金:国家杰出青年基金资助课题(30525043)~~
摘 要:目的探讨三七总皂苷(PNS)预处理对急性心肌缺血的作用。方法 SD大鼠ig给予PNS 25~800 mg·kg-1,每天2次连续7次,末次给药30 min后,结扎冠状动脉前降支缺血24 h。氯化三苯基四氮唑染色法测定心肌梗死面积,颈总动脉插管测定左心室内血流动力学变化,自动生化分析仪检测心肌酶谱。结果与急性心肌缺血模型组相比,PNS 50,100,200和400 mg·kg-1能显著降低心肌缺血大鼠的心肌梗死面积(P<0.05),降低心肌缺血后左心室舒张末压,提高左心室收缩压,增强等容收缩期左心室内压最大上升速率和等容舒张期左心室内压最大下降速率;显著降低血清中乳酸脱氢酶和肌酸激酶活性,降低α-羟丁酸脱氢酶和天冬氨酸氨基转移酶活性。结论 PNS在50~400 mg·kg-1剂量范围内能显著降低心肌缺血大鼠的心肌梗死面积,提高左心室舒张和收缩功能,明显抑制急性心肌缺血大鼠心肌酶的释放,具有改善心肌缺血的作用。OBJECTIVE To explore the effect of Panax notoginseng saponins (PNS) pretreatment on acute myocardial ischemia in rats. METHODS The rats were ig given PNS 0, 25, 50, 100, 200, 400, 600 and 800 mg·kg^-1, twice a day, for 7 times. After the last administration for 30 min, the acute myocardial ischemia model was induced by left anterior descending coronary artery ligation. The percentage of the myocardial infarct size was determined by TTC staining after 24 h, and left ventricular carotid artery blood flow dynamics was monitored by a biological signal acquisition and analysis system. Meanwhile, the cardiac enzymes related to myocardial infarction were assayed by an automatic biochemical analyzer. RESULTS Compared with model group, PNS 50, 100, 200 and 400 mg·kg^-1 pretreatment significantly reduced infarct size in myocardial ischemia rats, decreased left ventricular end-diastolic pressure, improved left ventricular systolic pressure, and increased the maximum rate of increase/decrease in left ventricular pressure. Serum levels of lactate dehydrogenase and creatine kinase were significantly lowered; α-hydroxybutyrate dehydrogenase and aspartate aminotransferase were also obviously decreased. CONCLUSION PNS 50 - 400 mg·kg^-1 could significantly reduce myocardial infarct size, improve left ventricular diastolic and systolic function and inhibit the release of myocardial enzymes.
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