Protective Effect of Catalpol on Myocardium in Rats with Isoprenaline-Induced Myocardial Infarcts via Angiogenesis through Endothelial Progenitor Cells and Notch1 Signaling Pathway

Protective Effect of Catalpol on Myocardium in Rats with Isoprenaline-Induced Myocardial Infarcts via Angiogenesis through Endothelial Progenitor Cells and Notch1 Signaling Pathway
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梓醇通过内皮祖细胞血管生成和 Notch1 信号通路对异丙肾上腺素诱发心肌梗塞大鼠心肌的保护作用

DOI:
10.4236/pp.2013.48088
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发表时间:
2013-11
期刊:
Pharmacology & Pharmacy
影响因子:
--
通讯作者:
童晓云
童晓云
中科院分区:
其他
文献类型:
--
作者:
童晓云

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通过异丙肾上腺素(INN)诱导大鼠急性心肌梗死模型,研究梓醇对内皮祖细胞、Notch 1信号通路及血管新生的影响。为分析梓醇对大鼠心肌的病理状态及影响,灌胃给药3周后,通过心电图证实心肌梗死,测定心肌组织乳酸脱氢酶(LDH)、丙二醛(MDA)、肌酸激酶(CK)和超氧化物歧化酶(SOD)的活性,并进一步进行HE和TTC染色分析,同时肉眼观察梗死面积。内皮祖细胞(EPCs)的流式细胞术研究表明,EPCs在梗死过程中被动员。采用免疫组化方法检测RBPjκ,Western blot方法检测Notch 1和Jagged 1在血管生成中的作用。结果表明,梓醇对大鼠脑梗死有保护作用,其机制可能与动员EPCs和激活Notch 1信号通路有关。
Protective effect of catalpol on myocardium was studied in relation to endothelial progenitor cells, Notch1 signaling pathway and angiogenesis in rats with isoprenaline (INN)-induced acute myocardial infarcts. To analyze the pathological status and impact of catalpol on the rats, 3 weeks after intragastric gavage, the animals were verified for myocardial infarcts with electrocardiogram and measured for enzyme activity of lactate dehydrogenase (LDH), malondialdehyde (MDA), creatine kinase (CK) and superoxide dismutase (SOD) in myocardium, and further analyzed using HE and TTC staining, as well as visual examination of infarct area. Flow cytometry study of endothelial progenitor cells (EPCs) indicated that the EPCs were mobilized during infarction. The roles of Notch1 signaling pathway in angiogenesis of the infracted animals were studied using immunohistochemistry analysis of RBPjκ and Western blot analysis of Notch1 and Jagged1. Our results obtained from the rats treated with catalpol, positive drug and control showed that catalpol could protect rats from infarction probably by mobilization of EPCs and activation of Notch1 signaling pathway.
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