Quercetin inhibits cardiomyocyte apoptosis via Sirt3/SOD2/mitochondrial reactive oxygen species during myocardial ischemia–reperfusion injury

• DOI: 10.1016/j.heliyon.2024.e39031
• Publication Date: 2024-10-05T16:15:02Z
• Authors: Da Xiong; Xin Wang; Haiyu Wang; Xia Chen; Hongrong Li; Yongwu Li; Minghua Zhong; Jingcheng Gao; Zicong Zhao; Wenjun Ren
• Keywords: SIRT3; SOD2; Mitochondrial ROS

BackgroundMyocardial ischemia/reperfusion injury (MI/RI) can lead to impaired cardiac function. Quercetin (Que) has a positive effect and improves MI/RI. Sirtuin-3 (Sirt3) is deacetylase that ameliorates oxidative stress associated with This study aimed investigate the molecular mechanism by which Que protects function against MI/RI through Sirt3 signaling pathway.MethodsWe conducted experiments constructing hypoxia/reoxygenation (H/R) cardiomyocytes rat models. H9C2 cells were transfected siRNA-Sirt3. Cardiomyocyte apoptosis was examined TUNEL Western blotting. The index also determined. Mitochondrial reactive oxygen species (ROS) activity assays, ATP assays mitochondrial membrane potential performed. Evans Blue/TTC staining used examine surviving myocardial tissue.ResultsIn constructed H/R animal models, it found cell increased (Bcl-2 expression downregulated; Bax cleaved caspase-3/8/9 upregulated). In addition, levels (MDA increased; SOD, CAT, GSH-Px decreased), tissue damaged (LDH, CK content increased), downregulated, acetylation of superoxide dismutase 2 (SOD2) (AC-SOD2), ROS increased. treatment alleviated effects on rats. upregulated, SOD2 decreased, production reduced treatment. After knocked down, we AC-SOD2 upregulated in cardiomyocytes, further degree injury, while attenuated knockdown cardiomyocytes.ConclusionQue inhibits cardiomyocyte apoptosis, reduces levels, prevents impairment during via Sirt3/SOD2/mitochondrial pathway.