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Original Research

Open Access

Artesunate inhibits ROS production and ameliorates mitochondrial damage through the SIRT1/FOXO3a/MnSOD pathway to alleviate heart failure

  • Yaping Li1
  • Peng Hu2,*,

1Department of Cardiology, Wuhan Third Hospital, Tongren Hospital of Wuhan University, 430074 Wuhan, Hubei, China

2Departement of Gynecological Oncology, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, 430079 Wuhan, Hubei, China

DOI: 10.22514/sv.2024.116 Vol.20,Issue 9,September 2024 pp.103-109

Submitted: 31 May 2024 Accepted: 09 July 2024

Published: 08 September 2024

*Corresponding Author(s): Peng Hu E-mail: hup0871@163.com

Abstract

Heart failure (HF) is a complex and multifactorial disease responsible for over 17.3 million deaths annually, primarily mediated by oxidative stress-induced mitochondrial dysfunction. Artesunate (AS), an artemisinin derivative, possesses anti-inflammatory and antioxidative properties and is used to enhance mitochondrial function and reduce reactive oxygen species (ROS) generation. However, its specific effects and mechanisms in HF remain poorly understood. In this study, we investigated the impact of AS on Doxorubicin hydrochloride (Dox)-induced injury in H9C2 cardiomyocytes. The results showed that AS promoted cell viability, decreased ROS production and mitigated mitochondrial damage in Dox-exposed H9C2 cells. Importantly, AS also modulated the Silent information regulator 1 (SIRT1)/Forkhead box O3a (FOXO3a)/Manganese superoxide dismutase (MnSOD) pathway, indicating its potential therapeutic utility in HF by inhibiting ROS production and preserving mitochondrial function in doxorubicin-treated H9C2 cardiomyocytes.


Keywords

Heart failure (HF); Artesunate (AS); Dox; Mitochondrial damage; SIRT1/FOXO3a/MnSOD pathway


Cite and Share

Yaping Li,Peng Hu. Artesunate inhibits ROS production and ameliorates mitochondrial damage through the SIRT1/FOXO3a/MnSOD pathway to alleviate heart failure. Signa Vitae. 2024. 20(9);103-109.

References

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