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Please use this identifier to cite or link to this item: https://ir.swu.ac.th/jspui/handle/123456789/13021
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dc.contributor.authorPhungphong S.
dc.contributor.authorKijtawornrat A.
dc.contributor.authorde Tombe P.P.
dc.contributor.authorWattanapermpool J.
dc.contributor.authorBupha-Intr T.
dc.contributor.authorSuksamrarn S.
dc.date.accessioned2021-04-05T03:22:01Z-
dc.date.available2021-04-05T03:22:01Z-
dc.date.issued2017
dc.identifier.issn10956670
dc.identifier.other2-s2.0-85020256751
dc.identifier.urihttps://ir.swu.ac.th/jspui/handle/123456789/13021-
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85020256751&doi=10.1002%2fjbt.21942&partnerID=40&md5=09ca837c52a5416a4bc27861793e15e0
dc.description.abstractThe 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 (IC50 of 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. © 2017 Wiley Periodicals, Inc.
dc.subjectadenosine triphosphatase (calcium)
dc.subjectadenosine triphosphatase (magnesium)
dc.subjectalpha mangostin
dc.subjectcalcium ion
dc.subjectdimethyl sulfoxide
dc.subjectsarcoplasmic reticulum calcium transporting adenosine triphosphatase
dc.subjectunclassified drug
dc.subjectxanthone derivative
dc.subjectmangostin
dc.subjectsarcoplasmic reticulum calcium transporting adenosine triphosphatase
dc.subjectxanthone derivative
dc.subjectadult
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectcardiac muscle cell
dc.subjectcell isolation
dc.subjectconcentration response
dc.subjectdose response
dc.subjectdrug dose comparison
dc.subjectdrug specificity
dc.subjectenzyme inhibition
dc.subjectheart left ventricle pressure
dc.subjectheart left ventricle relaxation
dc.subjectheart muscle relaxation
dc.subjectin vitro study
dc.subjectin vivo study
dc.subjectmale
dc.subjectnonhuman
dc.subjectrat
dc.subjectanimal
dc.subjectantagonists and inhibitors
dc.subjectcardiac muscle
dc.subjectdiastole
dc.subjectdrug effects
dc.subjectheart ventricle
dc.subjectLeporidae
dc.subjectmetabolism
dc.subjectpathophysiology
dc.subjectAnimals
dc.subjectDiastole
dc.subjectHeart Ventricles
dc.subjectMale
dc.subjectMyocardium
dc.subjectMyocytes, Cardiac
dc.subjectRabbits
dc.subjectSarcoplasmic Reticulum Calcium-Transporting ATPases
dc.subjectXanthones
dc.titleAcute inhibitory effect of alpha-mangostin on sarcoplasmic reticulum calcium-ATPase and myocardial relaxation
dc.typeArticle
dc.rights.holderScopus
dc.identifier.bibliograpycitationJournal of Biochemical and Molecular Toxicology. Vol 31, No.10 (2017)
dc.identifier.doi10.1002/jbt.21942
Appears in Collections:Scopus 1983-2021

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