Strawberry fruit (Fragaria x ananassa cv. Romina) extenuates iron-induced cardiac oxidative injury via effects on redox balance, angiotensin-converting enzyme, purinergic activities, and metabolic pathways

Abstract

The potential cardioprotective properties of strawberry fruit (Fragaria x ananassa) (SF) were investigated in cardiac tissues ex vivo. Oxidative injury was induced by incubating freshly harvested cardiac tissue homogenates from healthy Sprague Dawley male rats with 0.1 mM FeSO4 for 30 min at 37°C. The induction of oxidative injury resulted in depleted levels of glutathione, superoxide dismutase, catalase, E-NTPDase activities, and HDL-c, while elevating the levels of malondialdehyde, angiotensin-converting enzyme, acetylcholinesterase, ATPase, lipase activities, cholesterol, triglyceride, and LDL-c. Co-incubation with SF significantly reversed these levels and activities with concomitant depletion of oxidative-induced metabolites and reactivation of oxidative-inactivated pathways, while limiting beta-oxidation of very long chain fatty acids and mitochondrial beta-oxidation of medium-chain saturated fatty acids pathways. These data portray the potential cardioprotective effects of strawberry fruits against oxidative-induced cardiopathy via the attenuation of oxidative stress, inhibition of ACE and acetylcholinesterase activities, and modulation of lipid dysmetabolism.