Cardioprotective effect of gallic acid on cardiac troponin-T, cardiac marker enzymes, lipid peroxidation products and antioxidants in experimentally induced myocardial infarction in Wistar rats
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Abstract
Currently there has been an increased interest globally to identify antioxidant compounds
that are pharmacologically potent and have low or no side effects for use in preventive
medicine. This study was designed to evaluate the protective effect of gallic acid
on cardiac marker enzymes, troponin-T, LDH-isoenzyme pattern, lipid peroxidation products
and antioxidant status in isoproterenol (ISO)-induced myocardial infarction in male
Wistar rats. Male albino Wistar rats were pretreated with gallic acid (15 mg/kg) daily
for a period of 10 days. After the treatment period, ISO (100 mg/kg) was subcutaneously
injected to rats at an interval of 24 h for 2 days. ISO-induced myocardial damage
was indicated by increased activities of marker enzymes such as creatine kinase, creatine
kinase-MB, aspartate transaminase, alanine transaminase and lactate dehydrogenase
in serum and the levels of troponin-T in the serum. Increased LDH-isoenzyme bands
(LDH-1 and LDH-2) were also observed in serum of ISO-induced rats. In addition to
these diagnostic markers, the levels of lipid peroxidation products in plasma and
the heart were significantly (P<0.05) increased and the activities of enzymic antioxidants
such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase
and glutathione-S-transferase in the heart and non-enzymic antioxidants such as glutathione,
vitamin C and E in plasma and the heart were significantly (P<0.05) decreased in ISO-induced
rats. The level of uric acid in plasma was significantly (P<0.05) increased in ISO-treated
rats. Gallic acid pretreatment showed significant protective effect on all the biochemical
parameters studied. Histopathological findings of gallic acid pretreated myocardial
infarcted heart confirmed the biochemical findings of this study. Thus, gallic acid
protects the myocardium against isoproterenol-induced oxidative stress.