Neural Remodeling of the Left Atrium in rats by Rosuvastatin following Acute Myocardial Infarction

Author:

Wang Jiang-Rong1,Wang Meng-Zan2,Zheng Shao-Hua3,Li Zhi-Yuan1

Affiliation:

1. Department of Cardiology, The First Affiliated Hospital of Shandong First Medical University, Jinan, Shandong 250014, China

2. Department of Cardiology, People’s Hospital of Liaocheng, Liaocheng, Shandong 252000, China

3. Department of Cardiology, People’s Hospital of Dongying, Dongying, Shandong 25700, China

Abstract

AbstractObjectiveThis study aims to investigate the effect of rosuvastatin on sympathetic neural remodeling of the left atrium (LA) in rats after myocardial infarction (MI).MethodsRats were randomly divided into a three groups: sham group, statin group, and MI group. The mRNA expression levels of the growth-associated protein-43 (GAP43) and nerve growth factor (NGF) were measured by RT-PCR. Immunohistochemistry was used to detect the distribution and density of GAP43- and NGF-positive nerves. The expression levels of these proteins were quantified by Western blot.ResultsCompared with the sham group, the average optical density (AOD) values of GAP43 and nerve growth factor (NGF)-positive substances in the LA in the statin and MI groups were significantly higher (P<0.01), but the AOD values in the statin group were lower than of those in the MI group (P<0.01). Furthermore, the AOD values of GAP43 and NGF positive nerves in the left stellate ganglion in the statin and MI groups were significantly higher (P<0.01), but the AOD values in the statin group were lower, when compared with the MI group (P<0.01).ConclusionRosuvastatin could effectively improve the sympathetic neural remodeling of LA in MI rats.

Publisher

Walter de Gruyter GmbH

Subject

General Agricultural and Biological Sciences,General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Neuroscience

Reference40 articles.

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3. The effect of early and intensive statin therapy on ventricular premature beat or non-sustained ventricular tachycardia in patients with acute coronary syndrome;Cardiol J,2010

4. Nerve growth factor-induced Akt/mTOR activation protects the ischemic heart via restoring autophagic flux and attenuating ubiquitinated protein accumulation;Oncotarget,2017

5. Activin A inhibition attenuates sympathetic neural remodelingfollowing myocardial infarction in rats;Mol Med Rep,2018

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