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首页> 外文期刊>Naunyn-Schmiedeberg's Archives of Pharmacology >Investigation of therapeutic potential and molecular mechanism of vitamin P and digoxin in I/R-induced myocardial infarction in rat.
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Investigation of therapeutic potential and molecular mechanism of vitamin P and digoxin in I/R-induced myocardial infarction in rat.

机译:维生素P和地高辛在I / R诱发的大鼠心肌梗死中的治疗潜力和分子机制研究。

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摘要

Ischemic-reperfusion (I/R) is a major event in the pathogenesis of ischemic heart disease that leads to higher rate of mortality. The study has been designed to investigate the therapeutic potential and molecular mechanism of vitamin P and digoxin in I/R-induced myocardial infarction in isolated rat heart preparation by using Langendorff apparatus. The animals were treated with vitamin P (50 and 100?mg/kg; p.o.) and digoxin (500?μg/kg) for 5 consecutive days. Digoxin served as a positive control in the present study. On the sixth day, the heart was harvested and induced to 30?min of global ischemia followed by 120?min of reperfusion using Langendorff apparatus. The coronary effluent was collected at different time intervals (i.e. basal, 1, 15, 30, 45, 60 and 120?min.) for the assessment of myocardial contractility function. In addition, creatine kinase-M and B subunits (CK-MB), lactate dehydrogenase (LDH1) and Na(+)-K(+)-ATPase activity along with oxidative tissue biomarkers (i.e. thio-barbituric acid reactive substances (TBARS) and reduced glutathione (GSH)) changes were estimated. The I/R of myocardium produced decrease in coronary flow rate; increase in CK-MB, LDH1 and Na(+)-K(+)-ATPase activity along with increase in TBARS and decrease in GSH levels as compared to normal group. The treatment with vitamin P (100?mg/kg) and digoxin (500?μg/kg) have produced a significant (p?
机译:缺血再灌注(I / R)是缺血性心脏病发病机理中的一个重大事件,可导致更高的死亡率。本研究旨在通过Langendorff装置研究离体大鼠心脏制剂中维生素P和地高辛在I / R诱发的心肌梗塞中的治疗潜力和分子机制。连续5天用维生素P(50和100?mg / kg;口服)和地高辛(500?μg/ kg)处理动物。地高辛在本研究中作为阳性对照。第六天,收获心脏并诱导30分钟的局部缺血,然后用Langendorff仪器再灌注120分钟。在不同的时间间隔(即基础,1、15、30、45、60和120分钟)收集冠状流出物,以评估心肌的收缩功能。此外,肌酸激酶M和B亚基(CK-MB),乳酸脱氢酶(LDH1)和Na(+)-K(+)-ATPase活性以及氧化性组织生物标志物(即硫代巴比妥酸反应性物质(TBARS))并估计减少的谷胱甘肽(GSH)变化。心肌的I / R降低了冠状动脉流速;与正常组相比,CK-MB,LDH1和Na(+)-K(+)-ATPase活性增加,TBARS增加,GSH水平降低。维生素P(100?mg / kg)和地高辛(500?μg/ kg)处理对I / R引起的上述功能,代谢和组织生物标志物变化产生了显着的改善作用(p <0.05)。维生素P具有改善I / R诱导的心肌功能变化的潜力。这可能是由于其自由基清除和通过抑制Na(+)-K(+)-ATPase活性而具有的抗梗塞特性。因此,它可用作治疗心血管疾病的潜在治疗药物。

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