Sukanya PhungphongAnusak KijtawornratPieter P. de TombeJonggonnee WattanapermpoolTepmanas Bupha-IntrSunit SuksamrarnMahidol UniversityChulalongkorn UniversityLoyola University Stritch School of MedicineSrinakharinwirot University2018-12-212019-03-142018-12-212019-03-142017-10-01Journal of Biochemical and Molecular Toxicology. Vol.31, No.10 (2017)10990461109566702-s2.0-85020256751https://repository.li.mahidol.ac.th/handle/123456789/41802© 2017 Wiley Periodicals, Inc. The benefits of α-mangostin for various tissues have been reported, but its effect on the heart has not been clarified. This study aimed to evaluate the effects of α-mangostin on cardiac function. Using a cardiac sarcoplasmic reticulum (SR) membrane preparation, α-mangostin inhibited SR Ca2+-ATPase activity in a dose-dependent manner (IC50of 6.47 ± 0.7 μM). Its suppressive effect was specific to SR Ca2+-ATPase but not to myofibrillar Ca2+-ATPase. Using isolated cardiomyocytes, 50 μM of α-mangostin significantly increased the duration of cell relengthening and increased the duration of Ca2+transient decay, suggesting altered myocyte relaxation. The relaxation effect of α-mangostin was also supported in vivo after intravenous infusion. A significant suppression of both peak pressure and rate of ventricular relaxation (–dP/dt) relative to DMSO infusion was observed. The results from the present study demonstrated that α-mangostin exerts specific inhibitory action on SR Ca2+-ATPase activity, leading to myocardial relaxation dysfunction.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyEnvironmental ScienceArticleSCOPUS10.1002/jbt.21942