Objective: To investigate and compare the protective effects of Astragaloside IV (AST) and Quercetin (QUE) on rat myocardial cells after their exposure to hypoxia, and to determine their dose-effect relationship.
Methods: Myocardial cells from fetal SD rat were cultured in vitro and divided into 7 groups: i.e. A (hypoxia), B (hypoxia and 100 mg/L of QUE), C (hypoxia and 50 mg/L of QUE), D (hypoxia and 25 mg/L of QUE), E (hypoxia and 50.0 mg/L of AST), F (hypoxia and 25.0 mg/L of AST), G (hypoxia and 12.5 mg/L AST) H(hypoxia and 10 mg/L of VitE) groups. Different doses of AST and QUE were added into the culture media cells in each group before the myocardial cells receiving hypoxia for 12 hrs. The number of viable cells (CCK-8) and the content of lactate dehydrogenase (LDH), superoxide dismutase (SOD), malondialdehyde (MDA), active oxygen (ROS, with detection only in A, C, F and H groups) were determined after hypoxia.
Results: The amount of LDH, MDA, ROS (C, F groups) in group B - G decreased significantly compared with those of group A, while the number of viable cells and the SOD content increased significantly. The protective effects were better in group B - G than that of the group H. With the same dosage, levels of LDH, CCK-8 in AST-treated groups were significantly lower than those in QUE-treated group (the number of viable cells in group C, F was 0.454 +/- 0.018, 0.471 +/- 0.017, and the content of lactate dehydrogenase was 2800 +/- 9,2312 +/- 52). There were no significant differences in MDA, SOD and ROS levels between AST and QUE treated groups (ROS in C and F groups were 16.0 +/- 5.3 vs 22.4 +/- 8.7, P > 0.05).
Conclusion: AST and QUE might be beneficial in the protection of myocardial cells against hypoxia because of attenuation of oxidative damage. The protective effects of both AST and QUE are better than that of VitE, and that of AST is better than QUE as shown by a decrease in the amount of LDH and increase in the number of viable cells with the same dosage, but no obvious difference is shown between them in attenuating oxidative damage.
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Cardiovasc Toxicol
December 2024
Department of Cardiovascular Center, Beijing Tongren Hospital, Capital Medical University, No. 3 Chongwenmennei Street, Dongcheng District, Beijing, 100730, China.
Nuclear factor erythroid 2-related factor 2 (NRF2) is a redox-sensitive transcriptional factor that enables cells to resist oxidant responses, ferroptosis and inflammation. Here, we set out to probe the effects of NRF2 on cardiomyocyte injury under acute myocardial infarction (AMI) condition and its potential mechanism. Human cardiomyocytes were exposed to hypoxia/reoxygenation (H/R) to induce cell injury.
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December 2024
Department of Cardiology, Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China.
Introduction: Patients with acute myocardial infarction (AMI) are at high risk of progressing to heart failure (HF). Recent research has shown that lipid droplet-related genes (LDRGs) play a crucial role in myocardial metabolism following MI, thereby influencing the progression to HF.
Methods: Weighted gene co-expression network analysis (WGCNA) and differential expression gene analysis were used to screen a transcriptome dataset of whole blood cells from AMI patients with (AMI HF, = 16) and without progression (AMI no-HF, = 16).
Front Cell Dev Biol
December 2024
Institute of Precision Medicine, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Introduction: Sepsis-induced cardiomyopathy is a common complication of sepsis and is associated with higher mortality. To date, effective diagnostic and management strategies are still lacking. Recent studies suggest that ferroptosis plays a critical role in sepsis-induced cardiomyopathy and ferroptosis inhibitor Ferrostatin-1 (Fer-1) improved cardiac dysfunction and survival in lipopolysaccharide (LPS) induced endotoxemia.
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
December 2024
Fifth Clinical Medical College of Shanxi Medical University, Taiyuan 030012, China.
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Pharmacol Res
December 2024
Pathologie, School for Cardiovascular Diseases, Fac. Health, Medicine and Life Sciences, Maastricht university, MUMC, Netherland. Electronic address:
Wnt and Notch signaling pathways play crucial roles in the development and homeostasis of the cardiovascular system. These pathways regulate important cellular processes in cardiomyocytes, endothelial cells, and smooth muscle cells, which are the key cell types involved in the structure and function of the heart and vasculature. During embryonic development, Wnt and Notch signaling coordinate cell fate specification, proliferation, differentiation, and morphogenesis of the heart and blood vessels.
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