Rooibos extracts, including its derived polyphenolic compounds, are increasingly explored for their ameliorative effects against diabetes-associated complications. An extract of ‘fermented’ (oxidized) rooibos (FRE) can protect cardiomyocytes from diabetic rats against oxidative stress-induced damage, however, its mechanism of action remains unknown. Using an established model of H9c2 cardiomyocytes exposed to high glucose concentrations, the current study elaborates on mechanisms associated with the cardioprotective effects of FRE, especially its impact on mitochondrial energetics and capacity to enhance intracellular antioxidants under hyperglycemic conditions. The results showed that exposure of H9c2 cardiomyocytes to elevated glucose concentrations induced a state of myocardial substrate inflexibility, characterized by altered free fatty acid (FFA) uptake and oxidation, followed by impaired mitochondrial energetics and accelerated oxidative stress-induced cardiac damage. Our data revealed that FRE ameliorated high glucose-induced abnormalities to a similar degree as metformin. Here FRE treatment improved FFA utilization and enhanced levels of intracellular antioxidants such as glutathione and superoxide dismutase. These are the first results to show that FRE can control cardiac mitochondrial energetics under stimulated hyperglycemic conditions. Of significant interest was the ability of FRE to enhance intracellular coenzyme Q9 levels, a major component of the electron transport chain that plays a crucial role in maintaining efficient aerobic respiration and counteracting oxidative stress. The current results enhance our understanding of the potential protective properties of FRE against high glucose-induced cardiac damage, and also provides impetus for more studies to investigate the modulatory effect of FRE on mitochondrial-linked pathological abnormalities.

Fermented rooibos extract attenuates hyperglycemia-induced myocardial oxidative damage by improving mitochondrial energetics and intracellular antioxidant capacity / Dludla, P. V.; Johnson, R.; Mazibuko-Mbeje, S. E.; Muller, C. J. F.; Louw, J.; Joubert, E.; Orlando, P.; Silvestri, S.; Chellan, N.; Nkambule, B. B.; Essop, M. F.; Tiano, L.. - In: SOUTH AFRICAN JOURNAL OF BOTANY. - ISSN 0254-6299. - 131:(2020), pp. 143-150. [10.1016/j.sajb.2020.02.003]

Fermented rooibos extract attenuates hyperglycemia-induced myocardial oxidative damage by improving mitochondrial energetics and intracellular antioxidant capacity

Orlando P.;Silvestri S.;Tiano L.
2020-01-01

Abstract

Rooibos extracts, including its derived polyphenolic compounds, are increasingly explored for their ameliorative effects against diabetes-associated complications. An extract of ‘fermented’ (oxidized) rooibos (FRE) can protect cardiomyocytes from diabetic rats against oxidative stress-induced damage, however, its mechanism of action remains unknown. Using an established model of H9c2 cardiomyocytes exposed to high glucose concentrations, the current study elaborates on mechanisms associated with the cardioprotective effects of FRE, especially its impact on mitochondrial energetics and capacity to enhance intracellular antioxidants under hyperglycemic conditions. The results showed that exposure of H9c2 cardiomyocytes to elevated glucose concentrations induced a state of myocardial substrate inflexibility, characterized by altered free fatty acid (FFA) uptake and oxidation, followed by impaired mitochondrial energetics and accelerated oxidative stress-induced cardiac damage. Our data revealed that FRE ameliorated high glucose-induced abnormalities to a similar degree as metformin. Here FRE treatment improved FFA utilization and enhanced levels of intracellular antioxidants such as glutathione and superoxide dismutase. These are the first results to show that FRE can control cardiac mitochondrial energetics under stimulated hyperglycemic conditions. Of significant interest was the ability of FRE to enhance intracellular coenzyme Q9 levels, a major component of the electron transport chain that plays a crucial role in maintaining efficient aerobic respiration and counteracting oxidative stress. The current results enhance our understanding of the potential protective properties of FRE against high glucose-induced cardiac damage, and also provides impetus for more studies to investigate the modulatory effect of FRE on mitochondrial-linked pathological abnormalities.
2020
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11566/285722
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