Article Publish Status: FREE
Abstract Title:

Aspalathin Protects the Heart against Hyperglycemia-Induced Oxidative Damage by Up-Regulating Nrf2 Expression.

Abstract Source:

Molecules. 2017 Jan 14 ;22(1). Epub 2017 Jan 14. PMID: 28098811

Abstract Author(s):

Phiwayinkosi V Dludla, Christo J F Muller, Elizabeth Joubert, Johan Louw, M Faadiel Essop, Kwazi B Gabuza, Samira Ghoor, Barbara Huisamen, Rabia Johnson

Article Affiliation:

Phiwayinkosi V Dludla


Aspalathin (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-regulatingexpression in H9c2 cardiomyocytes and diabetic (/) 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 ofabolished this protective response of ASP and exacerbated cardiomyocyte apoptosis./mice and their non-diabetic (/) 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/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 ofand its downstream antioxidant genes. These results indicate that ASP maintains cellular homeostasis and protects the myocardium against hyperglycemia-induced oxidative stress through activation ofand its downstream target genes.

Study Type : Animal Study

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