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Tanshinone IIA attenuates heart failure via inhibiting oxidative stress in myocardial infarction rats

  • Authors:
    • Ruijuan Chen
    • Wenli Chen
    • Xiaoling Huang
    • Qinglin Rui
  • View Affiliations / Copyright

    Affiliations: Emergency Department, Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, Nanjing, Jiangsu 210029, P.R. China, Department of Rehabilitation Medicine, Zhongda Hospital Southeast University, Nanjing, Jiangsu 210009, P.R. China
    Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 404
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    Published online on: March 26, 2021
       https://doi.org/10.3892/mmr.2021.12043
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Abstract

The purpose of the present study was to evaluate whether tanshinone IIA (TIIA) could treat cardiac dysfunction and fibrosis in heart failure (HF) by inhibiting oxidative stress. An HF model was induced by ligation of the left anterior descending artery to cause ischemia myocardial infarction (MI) in Sprague‑Dawley rats. Cardiac fibrosis was evaluated using Masson's staining, and the levels of collagen I, collagen III, TGF‑β, α‑smooth muscle actin (α‑SMA), matrix metalloproteinase (MMP) 2 and MMP9 were determined using PCR or western blotting. TIIA treatment reversed the decreases of left ventricular (LV) ejection fraction, fractional shortening (FS), LV systolic pressure and the maximum of the first differentiation of LV pressure (LV ± dp/dtmax), the increases of LV volume in systole, LV volume in diastole, LV end‑systolic diameter and LV end‑diastolic diameter in MI rats. TIIA administration also reversed the increases of expression levels of collagen I, collagen III, TGF‑β, α‑SMA, MMP2 and MMP9 in the heart of MI rats and in angiotensin (Ang) II‑treated cardiac fibroblasts (CFs). TIIA reversed the decreases of superoxide dismutase activity and malondialdehyde and the increases of superoxide anions and NADPH oxidase (Nox) activity in both MI rats and Ang II‑treated CFs. Nox4 overexpression inhibited the effects of TIIA of improving cardiac dysfunction and fibrosis in MI rats and Ang II‑treated CFs. These results demonstrated that TIIA improved cardiac dysfunction and fibrosis via inhibiting oxidative stress in HF rats. Nox4 could regulate the inhibitory effects of TIIA on HF and cardiac fibrosis.
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Copy and paste a formatted citation
Spandidos Publications style
Chen R, Chen W, Huang X and Rui Q: Tanshinone IIA attenuates heart failure via inhibiting oxidative stress in myocardial infarction rats. Mol Med Rep 23: 404, 2021.
APA
Chen, R., Chen, W., Huang, X., & Rui, Q. (2021). Tanshinone IIA attenuates heart failure via inhibiting oxidative stress in myocardial infarction rats. Molecular Medicine Reports, 23, 404. https://doi.org/10.3892/mmr.2021.12043
MLA
Chen, R., Chen, W., Huang, X., Rui, Q."Tanshinone IIA attenuates heart failure via inhibiting oxidative stress in myocardial infarction rats". Molecular Medicine Reports 23.6 (2021): 404.
Chicago
Chen, R., Chen, W., Huang, X., Rui, Q."Tanshinone IIA attenuates heart failure via inhibiting oxidative stress in myocardial infarction rats". Molecular Medicine Reports 23, no. 6 (2021): 404. https://doi.org/10.3892/mmr.2021.12043
Copy and paste a formatted citation
x
Spandidos Publications style
Chen R, Chen W, Huang X and Rui Q: Tanshinone IIA attenuates heart failure via inhibiting oxidative stress in myocardial infarction rats. Mol Med Rep 23: 404, 2021.
APA
Chen, R., Chen, W., Huang, X., & Rui, Q. (2021). Tanshinone IIA attenuates heart failure via inhibiting oxidative stress in myocardial infarction rats. Molecular Medicine Reports, 23, 404. https://doi.org/10.3892/mmr.2021.12043
MLA
Chen, R., Chen, W., Huang, X., Rui, Q."Tanshinone IIA attenuates heart failure via inhibiting oxidative stress in myocardial infarction rats". Molecular Medicine Reports 23.6 (2021): 404.
Chicago
Chen, R., Chen, W., Huang, X., Rui, Q."Tanshinone IIA attenuates heart failure via inhibiting oxidative stress in myocardial infarction rats". Molecular Medicine Reports 23, no. 6 (2021): 404. https://doi.org/10.3892/mmr.2021.12043
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