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

Yaping Li; Peng Hu

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 doxorubicintreated H9C2 cardiomyocytes.

ARTEMISININ derivatives; REACTIVE oxygen species; CELL survival; HEART failure; SUPEROXIDE dismutase

Signa Vitae, 2024, Vol 20, Issue 9, p103

1334-5605

Academic Journal

10.22514/sv.2024.116