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.

在铁诱导的心脏毒性中，研究了咖啡酸对血管紧张素转化酶（ACE）和嘌呤能酶活性以及糖异生的保护作用。0.1 mM FeSO ₄在健康雄性SD大鼠的心脏组织中诱发心脏毒性。通过将心脏组织与咖啡酸和0.1 mM FeSO ₄共同孵育来进行治疗。心脏毒性诱导显着（p  <0.05）耗尽了GSH水平，SOD，过氧化氢酶和ENTPDase活性，同时丙二醛（MDA），一氧化氮，ACE，ATPase，糖原磷酸化酶，葡萄糖6磷酸酶，果糖6- Biphsophatase和脂肪酶的活动。有显着性（p <0.05）这些水平的逆转以及使用咖啡酸治疗的活性。咖啡酸还会导致心脏胆固醇，甘油三酸酯，LDL-c水平下降，同时升高HDL-c水平。我们的结果表明，咖啡因具有抑制氧化不平衡和ACE活性的能力，同时还调节核苷酸水解和代谢转换，因此具有抗铁介导的心脏毒性的保护作用。