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作 者:李亮 姬艳苏[2] LI Liang;JI Yansu(General Hospital,Tianjin Medical University,Tianjin 300052,China;Affiliated Hospital of Logistics University of Chinese People忆s Armed Police Forces)
机构地区:[1]天津医科大学总医院,天津300052 [2]武警后勤学院附属医院
出 处:《西部中医药》2018年第9期17-20,共4页Western Journal of Traditional Chinese Medicine
基 金:天津市应用基础与前沿技术研究计划(编号14JCQNJC13600)
摘 要:目的:探讨黄芪总皂苷对心肌梗死后心力衰竭大鼠心肌酪氨酸激酶2/信号传导及转录激活因子3(JAK2/STAT3) mRNA和蛋白表达的影响。方法:复制心肌梗死后慢性心力衰竭大鼠模型,采用酶联免疫吸附法(ELI SA)检测血清氮末端-前体脑钠肽(NT-proBNP)含量变化,Ⅷ因子染色法观察心肌微血管数目,实时荧光定量PCR技术观察羧基端活性段脑钠肽(BNP)、JAK2和STAT3 mRNA水平,并用蛋白免疫印迹(West ern-Bl ot)技术观察心肌JAK2和STAT3蛋白水平的表达以及黄芪总皂苷的干预作用。结果:黄芪总皂苷能增加心肌微血管密度,下调心肌梗死后心力衰竭大鼠心肌组织JAK2在mRNA水平的表达,上调STAT3 mRNA和蛋白水平。结论:调节JAK2/STAT3可能是黄芪总皂苷抗心力衰竭,改善心肌供血,促进血管新生的机制之一。Objective: To discuss the effects of total saponins of HuangQi (Astragalus mongholicus) onJAK2/STAT3 mRNA and protein expressions of the rats with heart failure after myocardial infarction. Methods: Ratmodel with chronic heart failure (CHF) after myocardial infarction was duplicated, the contents of NT-proBNP weredetected by ELISA method, the number of myocardial microvessels was observed by VIII factor staining, the levelsof BNP, JAK2 and STAT3 mRNA were observed by real-time fluorescence quantitative PCR technology, theintervention effects of total saponins of HuangQi and the expressions of JAK2 and STAT3 protein were observed byWestern-Blot skills. Results: Total saponins of HuangQi could increase myocardial microvessel density, decrease theexpressions of JAK2 mRNA in myocardial tissue of the rats suffering CHF after myocardial infarction, and raise thelevels of STAT3 mRNA and protein. Conclusion: Regulating JAK2/STAT3 might be one of the mechanisms of totalsaponins of HuangQi fighting against heart failure, improvingmyocardial blood supply and promoting the angiogenesis.
关 键 词:慢性心力衰竭 JAK2/STAT3 黄芪总皂苷
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