Open Access

Renal sympathetic denervation alleviates myocardial fibrosis following isoproterenol-induced heart failure

  • Authors:
    • Neng Wang
    • Xiaoxin Zheng
    • Jin Qian
    • Wei Yao
    • Lu Bai
    • Guo Hou
    • Xuan Qiu
    • Xiaoyan Li
    • Xuejun Jiang
  • View Affiliations

  • Published online on: August 16, 2017     https://doi.org/10.3892/mmr.2017.7255
  • Pages: 5091-5098
  • Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The aim of the present study was to determine if renal sympathetic denervation (RSD) may alleviate isoproterenol-induced left ventricle remodeling, and to identify the underlying mechanism. A total of 70 rats were randomly divided into control (n=15), sham operation (n=15), heart failure (HF) with sham operation (HF + sham; n=20) and HF with treatment (HF + RSD; n=20) groups. The HF model was established by subcutaneous injection of isoproterenol; six weeks later, 1eft ventricular internal diameter at end‑systole (LVIDs), left ventricular systolic posterior wall thickness (LVPWs), 1eft ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were measured. Plasma norepinephrine (NE), angiotensin II (Ang II) and aldosterone (ALD) levels were measured by ELISA. Myocardial collagen volume fraction (CVF) was determined by Masson's staining. Reverse transcription‑quantitative polymerase chain reaction was used to determine the mRNA expression levels of ventricular transforming growth factor‑β (TGF‑β), connective tissue growth factor (CTGF) and microRNAs (miRs), including miR‑29b, miR‑30c and miR‑133a. The results demonstrated that LVIDs and LVPWs in the HF + RSD group were significantly decreased compared with the HF + sham group. By contrast, LVFS and LVEF in the HF + RSD group were significantly increased compared with the HF + sham group. RSD significantly reduced the levels of plasma NE, Ang II and ALD. CVF in the HF + RSD group was reduced by 38.1% compared with the HF + sham group. Expression levels of TGF‑β and CTGF were decreased, whereas those of miR‑29b, miR‑30c and miR‑133a were increased, in the HF + RSD group compared with the HF + sham group. These results indicated that RSD alleviates isoproterenol‑induced left ventricle remodeling potentially via downregulation of TGF‑β/CTGF and upregulation of miR‑29b, miR‑30c and miR‑133a. RSD may therefore be an effective non‑drug therapy for the treatment of heart failure.

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October-2017
Volume 16 Issue 4

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Copy and paste a formatted citation
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Spandidos Publications style
Wang N, Zheng X, Qian J, Yao W, Bai L, Hou G, Qiu X, Li X and Jiang X: Renal sympathetic denervation alleviates myocardial fibrosis following isoproterenol-induced heart failure. Mol Med Rep 16: 5091-5098, 2017
APA
Wang, N., Zheng, X., Qian, J., Yao, W., Bai, L., Hou, G. ... Jiang, X. (2017). Renal sympathetic denervation alleviates myocardial fibrosis following isoproterenol-induced heart failure. Molecular Medicine Reports, 16, 5091-5098. https://doi.org/10.3892/mmr.2017.7255
MLA
Wang, N., Zheng, X., Qian, J., Yao, W., Bai, L., Hou, G., Qiu, X., Li, X., Jiang, X."Renal sympathetic denervation alleviates myocardial fibrosis following isoproterenol-induced heart failure". Molecular Medicine Reports 16.4 (2017): 5091-5098.
Chicago
Wang, N., Zheng, X., Qian, J., Yao, W., Bai, L., Hou, G., Qiu, X., Li, X., Jiang, X."Renal sympathetic denervation alleviates myocardial fibrosis following isoproterenol-induced heart failure". Molecular Medicine Reports 16, no. 4 (2017): 5091-5098. https://doi.org/10.3892/mmr.2017.7255