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

Jing Zeng, Feng Huang, Yuangqing Tu, Saichun Wu, Manping Li, Xiaoyun Tong

College of Pharmacy, Jinan University, Guangzhou, Chin.
College of Pharmacy, Jinan University, Guangzhou, China.
College of Pharmacy, Jinan University, Guangzhou, China;.
Teaching & Research Section of Internal Medicine of Traditional Chi-nese Medicine, College of Clinical Medicine, Yunnan University of TCM, Kuming, China..

DOI: 10.4236/pp.2013.48088                

Abstract

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.

Keywords

Myocardial Infarction; Endothelial Progenitor Cell; Notch1 Signaling Pathway; Angiogenesis; Catalpol

Conflicts of Interest

The authors declare no conflicts of interest.

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