Ameliorative potential of ferulic acid on cardiotoxicity induced by mercuric chloride

Cardiovascular disease affects more people and causes more death commonly. Heart failure mainly occurs due to myocardial infarction and it may be associated with an antioxidant deficit as well as increased myocardial oxidative stress. The aim of the present study was designed to evaluate the myocardial infarction induced by mercuric chloride and the productive role of ferulic acid in rats. At sub-lethal dose of mercury chloride (1.30 mg/kg body weight 45 days daily) administered in rat, heart tissue shows an elevated level of lipid peroxidation (LPO) content and simultaneously decreased level of cardiac marker enzymes. Occurrence of cardiotoxicity is mainly due to the accumulation of heavy metal in cardiac tissues and increase in the level of blood serum specific markers. The following serum enzymes were drastically increased. Due to the mercury toxicity, the level of alkaline phosphatase (ALP), alanine transferase (ALT), aspartate transaminasas (AST), creative phosphokinase (CPK), total cholesterol (TC) and lactate dehydrogenase (LDH) were increased. The administration of sub-lethal dose of ferulic acid (5 mg/kg body weight 45 days daily) restores all the serum marker enzymes to near-normal level. This result suggests that the administration of ferulic acid not only promotes the marker enzymes but it also acts as a protective effect of cardiac tissues against mercury chloride-induced oxidative stress.