Caffeic Acid Protects against Iron-Induced Cardiotoxicity by Suppressing Angiotensin-Converting Enzyme Activity and Modulating Lipid Spectrum, Gluconeogenesis and Nucleotide Hydrolyzing Enzyme Activities

The protective effects of caffeic acid on angiotensin-converting enzyme (ACE) and purinergic enzyme activities, as well as gluconeogenesis was investigated in iron-induced cardiotoxicity. Cardiotoxicity was induced in heart tissues harvested from healthy male SD rats by 0.1 mM FeSO4. Treatment was carried out by co-incubating hearts tissues with caffeic acid and 0.1 mM FeSO4. Cardiotoxicity induction significantly (p < 0.05) depleted GSH level, SOD, catalase, and ENTPDase activities, with concomitant elevation of the levels of malondialdehyde (MDA), nitric oxide, ACE, ATPase, glycogen phosphorylase, glucose 6-phosphatase, fructose 6-biphsophatase, and lipase activities. There was significant (p < 0.05) reversion in these levels and activities on treatment with caffeic acid. Caffeic acid also caused depletion in cardiac levels of cholesterol, triglyceride, LDL-c, while elevating HDL-c level. Our results suggest the protective effect of caffeic acid against iron-mediated cardiotoxicity as indicated by its ability to suppress oxidative imbalance and ACE activity, while concomitantly modulating nucleotide hydrolysis and metabolic switch.

Automated summary

The study suggests that caffeic acid has a protective effect against iron-induced cardiotoxicity by suppressing oxidative imbalance and ACE activity, while modulating nucleotide hydrolysis and metabolic switch.