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作 者:刘丹[1] 王颖[1] 陈和平[1] 黄起壬[1] 何明[1]
机构地区:[1]南昌大学药学院药理学与分子治疗学系,南昌330006
出 处:《中药药理与临床》2009年第3期14-18,共5页Pharmacology and Clinics of Chinese Materia Medica
摘 要:目的:研究阿魏酸钠(SF)对离体大鼠心脏急性缺氧/复氧(A/R)损伤的药理性预适应延迟保护作用及其与缓激肽的关系。方法:6组Wistar大鼠分别为对照(Cont)组、A/R组、缺氧预适应(APC)组、APC+HOE140组、SF组、SF+HOE140组。SF组、SF+HOE140组大鼠静脉注射SF10mg/kg;25h后取大鼠心脏行Langendorff逆行灌流、制作A/R损伤模型。实验结束后分别检测LVP、±dp/dtmax等心功能指标、表面心电图、CF量以及其中LDH、CPK活性、心肌组织MDA含量与GSH-Px、SOD活性、心肌梗塞面积、心肌组织超微结构改变。结果:SF预处理能显著提高大鼠心脏LVP、±dp/dtmax、CF,降低LDH、CPK活性,SOD活性、GSH-Px活性增加,MDA含量减少;大鼠心脏梗塞面积明显减少。HOE140能取消SF预处理的上述延迟保护作用。结论:SF预处理对心肌组织急性A/R损伤有明显的延迟保护作用,其机制与缓激肽系统活性增强有关。To investigate the preconditioning delayed effects and mechanisms of sodium ferulate (SF) on isolated rat heart subjected to anoxia-reoxygenation (A/R) injury. Methods: 48 adult male Wistar rats were divided into six groups : control, A/R, anoxia preconditioning (APC), APC + HOE140, SF, SF + HOE140. The rats of SF and SF + HOE140 groups were intravenously administered SF 10 mg/kg, while the rats ofother four groups were intravenously administered equal volume NS, respectively. After 25 hours, isolated rat hearts were perfused in Langendorff mode and subjected to A/R injury. The indexes of cardiac function such as ECG, left ventricular pressure( LVP),± dp/dtmax and CF volume were recorded. The activities of SOD, GSH-Px, LDH and CPK, the contents of MDA , the changes of uhrastructure in myocardium and the area of myocardial infarction were measured. Results : Pretreatment with SF decreased LDH activity, MDA contents, the area of myocardial infarction and arrhythmia, while increased the activities of SOD and GSH-Px, improved heart function and ultrastructure of myocardium. The delayed protective effects of SF were abolished by HOE140. Conclusion: SF can induce the delayed cardioproteetion against acute A/R injury and the mechanisms may be related with the enhancement of the activity of bradykinin system.
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