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Aspalathin protects the heart against hyperglycemia-induced oxidative damage by up-regulating Nrf2 expression

dc.contributor.authorDludla, Phiwayinkosi V.en_ZA
dc.contributor.authorMuller, Christo J. F.en_ZA
dc.contributor.authorJoubert, Elizabethen_ZA
dc.contributor.authorLouw, Johanen_ZA
dc.contributor.authorEssop, M. Faadielen_ZA
dc.contributor.authorGabuza, Kwazi B.en_ZA
dc.contributor.authorGhoor, Samiraen_ZA
dc.contributor.authorHuisamen, Barbaraen_ZA
dc.contributor.authorJohnson, Rabiaen_ZA
dc.date.accessioned2018-01-25T06:32:10Z
dc.date.available2018-01-25T06:32:10Z
dc.date.issued2017
dc.identifier.citationDludla, P. V., et al. 2017. Aspalathin protects the heart against hyperglycemia-induced oxidative damage by up-regulating Nrf2 expression. Molecules, 22(1):129, doi:10.3390/molecules22010129
dc.identifier.issn1420-3049 (online)
dc.identifier.otherdoi:10.3390/molecules22010129
dc.identifier.urihttp://hdl.handle.net/10019.1/103087
dc.descriptionCITATION: Dludla, P. V., et al. 2017. Aspalathin protects the heart against hyperglycemia-induced oxidative damage by up-regulating Nrf2 expression. Molecules, 22(1):129, doi:10.3390/molecules22010129.
dc.descriptionThe original publication is available at http://www.mdpi.com
dc.description.abstractAspalathin (ASP) can protect H9c2 cardiomyocytes against high glucose (HG)-induced shifts in myocardial substrate preference, oxidative stress, and apoptosis. The protective mechanism of ASP remains unknown. However, as one of possible, it is well known that phytochemical flavonoids reduce oxidative stress via nuclear factor (erythroid-derived 2)-like 2 (Nrf2) activation resulting in up-regulation of antioxidant genes and enzymes. Therefore, we hypothesized that ASP protects the myocardium against HG- and hyperglycemia-induced oxidative damage by up-regulating Nrf2 expression in H9c2 cardiomyocytes and diabetic (db/db) mice, respectively. Using an oxidative stress RT2 Profiler PCR array, ASP at a dose of 1 µM was demonstrated to protect H9c2 cardiomyocytes against HG-induced oxidative stress, but silencing of Nrf2 abolished this protective response of ASP and exacerbated cardiomyocyte apoptosis. Db/db mice and their non-diabetic (db/+) littermate controls were subsequently treated daily for six weeks with either a low (13 mg/kg) or high (130 mg/kg) ASP dose. Compared to nondiabetic mice the db/db mice presented increased cardiac remodeling and enlarged left ventricular wall that occurred concomitant to enhanced oxidative stress. Daily treatment of mice with ASP at a dose of 130 mg/kg for six weeks was more effective at reversing complications than both a low dose ASP or metformin, eliciting enhanced expression of Nrf2 and its downstream antioxidant genes. These results indicate that ASP maintains cellular homeostasis and protects the myocardium against hyperglycemia-induced oxidative stress through activation of Nrf2 and its downstream target genes.en_ZA
dc.description.urihttp://www.mdpi.com/1420-3049/22/1/129
dc.format.extent16 pages : illustrationsen_ZA
dc.language.isoen_ZAen_ZA
dc.publisherMDPIen_ZA
dc.subjectDiabetes mellitusen_ZA
dc.subjectAspalathinen_ZA
dc.subjectOxidative stressen_ZA
dc.subjectMyocardium -- Diseasesen_ZA
dc.titleAspalathin protects the heart against hyperglycemia-induced oxidative damage by up-regulating Nrf2 expressionen_ZA
dc.typeArticleen_ZA
dc.description.versionPublisher's versionen_ZA
dc.rights.holderAuthors retain copyrighten_ZA


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