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Updated: Mar 9, 2026
A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
Published on: July 13, 2018
(+)-Catechin prevents methylglyoxal-induced mitochondrial dysfunction and apoptosis in EA.hy926 cells
Tianyu Zhang1, Yingying Mu1, Mingqi Yang1
1a College of Veterinary Medicine, Northwest A&F University , Yangling , Shaanxi , China and.
Objective:
To investigate whether (+)-catechin, a strong antioxidant, can prevent methylglyoxal (MGO)-induced cytotoxicity and its mechanism.
Methods:
Cytotoxicity, apoptosis, reactive oxygen species (ROS) generation, hydrogen peroxide (H2O2) formation, mitochondrial membrane potential (MMP) and mitochondrial morphology were measured in EA.hy926 cells.
Result:
MGO (4 mM)-induced cytotoxicity was markedly inhibited by (+)-catechin (0.1-4 mM) in 24 h. 1 mM MGO-induced apoptotic cell death (44.7%) was significantly inhibited by 4 mM (+)-catechin (to 24.4%), 1 mM aminoguanidine (AG) (to 28.8%) or 4 mM N-acetylcysteine (NAC) (to 24.3%). (+)-Catechin (4 mM) or AG (4 mM) can inhibit the decrease of MMP induced by MGO (2-8 mM) in 3 h. (+)-Catechin (4 mM) or AG (4 mM) can inhibit MGO (4 mM)-induced mitochondrial swelling in 3 h. However, MGO (4 mM)-induced ROS and H2O2 generation was not prevented by (+)-catechin (4 mM).
Conclusions:
(+)-Catechin prevents MGO-induced cytotoxicity in EA.Hy926 cells through inhibiting apoptosis and mitochondrial damage.
