Astragaloside IV alleviates heart failure by regulating SUMO‑specific protease 1 Corrigendum in /10.3892/etm.2023.12021

Liu,Juan; Li,Ya; Bian,Xiyun; Xue,Na; Yu,Jiancai; Dai,Shipeng; Liu,Xiaozhi

doi:10.3892/etm.2021.10510

Astragaloside IV alleviates heart failure by regulating SUMO‑specific protease 1

Corrigendum in: /10.3892/etm.2023.12021

Authors:
- Juan Liu
- Ya Li
- Xiyun Bian
- Na Xue
- Jiancai Yu
- Shipeng Dai
- Xiaozhi Liu
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Affiliations: Department of Cardiology, Cangzhou Central Hospital, Cangzhou, Hebei 061000, P.R. China, Central Laboratory, The Fifth Central Hospital of Tianjin, Tianjin 300450, P.R. China
Published online on: July 28, 2021 https://doi.org/10.3892/etm.2021.10510
Article Number: 1076
Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The present study investigated whether the protective effect and mechanism of astragaloside IV (AS‑IV) on heart failure (HF) involves small ubiquitin‑like modifier (SUMO)‑specific protease 1 (Senp1). Mouse HF was established by aortic constriction, inducing pressure overload. The model was confirmed by echocardiography 6 weeks after surgery. Mice were randomly divided into control, HF, HF+AS‑IV, and AS‑IV groups. Ventricular function was examined by echocardiography. Morphological changes of myocardial tissues were examined by H&E staining. The protein levels of the apoptosis‑related proteins, cleaved caspase‑3, caspase‑3, Bcl2, Bax, and SUMO‑Senp1 were determined by Western blotting. H₂O₂ in isolated mitochondria and cells was determined by Amplex Red. A reactive oxygen species (ROS) detection kit determined ROS levels in isolated mitochondria and HL‑1 cells. JC‑1 reagent measured mitochondrial membrane potential (ΔΨm). Apoptosis of HL‑1 cells was examined by terminal deoxynucleotidyl transferase dUTP nick end labeling. Compared with the control group, the heart weight and heart mass/body weight ratio increased in the HF group (P<0.05). Furthermore, the ejection fraction and left ventricular shortening fraction decreased (P<0.05), while the left ventricular end‑diastolic diameter (LVID;d) and end‑systolic diameter (LVID;s) increased (P<0.05). Finally, mitochondrial ROS and H₂O₂ increased (P<0.05), while the ΔΨm decreased (P<0.05). However, AS‑IV improved the cardiac function of HF mice, decreased the level of ROS and H₂O₂ in the myocardium, suppressed the decrease in ΔΨm, and decreased the apoptosis of myocardial cells (P<0.05). AS‑IV also decreased the Senp1‑overexpression. Furthermore, in HL‑1 cells, Senp1‑overexpression significantly inhibited the protective effects of AS‑IV. AS‑IV decreased oxidative stress in cardiomyocytes, decreased mitochondrial damage, inhibited ventricular remodeling, and ultimately improved cardiac function by inhibiting HF‑induced Senp1‑overexpression. This mechanism provides a novel theoretical basis and clinical treatment for HF.

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