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BioMed Research International
Volume 2017 (2017), Article ID 3495021, 12 pages
https://doi.org/10.1155/2017/3495021
Research Article

Effect of Wenxin Granules on Gap Junction and MiR-1 in Rats with Myocardial Infarction

1Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China
2National Engineering Research Center for R&D of TCM Multi-Ingredient Drugs, Beijing 100079, China
3Beijing University of Chinese Medicine Institute for Cardiovascular Disease, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China

Correspondence should be addressed to Limin Chai; moc.liamtoh@iahcnimil

Received 16 January 2017; Accepted 20 August 2017; Published 28 September 2017

Academic Editor: Bo Zuo

Copyright © 2017 Aiming Wu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Myocardial infarction (MI) patients are at high risk of potential lethal arrhythmia. Gap junction and microRNA-1 (miR-1) are both arrhythmia generating conditions. The present study investigated whether Wenxin Granules (Wenxin-Keli, WXKL) could prevent potential lethal arrhythmia by improving gap junctions and miR-1 following MI. Male Sprague-Dawley rats were divided randomly into control, model, metoprolol, low dose WXKL, and high dose WXKL groups. The MI rat model was created by coronary artery ligation. Treatments were administrated intragastrically to the rats for 4 weeks. Conventional transmission electron microscopy was performed to observe the ultrastructure of gap junctions. Quantitative real-time PCR and western blotting were used to detect the expression of miR-1, protein kinase C (PKC), and related proteins. Additionally, a programmatic electrophysiological stimulation test was performed to detect the ventricular fibrillation threshold (VFT). WXKL protected the ultrastructure of the gap junctions and their constituent Cx43 by regulating miR-1 and PKC mediated signal transduction and increased the VFT significantly in the rat MI model. The results suggested that WXKL is an effective alternative medicine to prevent potentially lethal arrhythmia following MI.