Abstract

Cardamom is a popular spice that has been commonly used in cuisines for flavor since ancient times. It has copious health benefits such as improving digestion, stimulating metabolism, and exhibits antioxidant and anti-inflammatory effects. The current study investigated the effect of cardamom on hemodynamic, biochemical, histopathological and ultrastructural changes in isoproterenol (ISO)-induced myocardial infarction. Wistar male albino rats were randomly divided and treated with extract of cardamom (100 and 200 mg/kg per oral) or normal saline for 30 days with concomitant administration of ISO (85 mg/kg, subcutaneous) on 29th and 30th days, at 24 h interval. ISO injections to rats caused cardiac dysfunction evidenced by declined arterial pressure indices, heart rate, contractility and relaxation along with increased preload. ISO also caused a significant decrease in endogenous antioxidants, superoxide dismutase, catalase, glutathione peroxidase, depletion of cardiomyocytes enzymes, creatine kinase-MB, lactate dehydrogenase and increase in lipid peroxidation. All these changes in cardiac and left ventricular function as well as endogenous antioxidants, lipid peroxidation and myocyte enzymes were ameliorated when the rats were pretreated with cardamom. Additionally, the protective effects were strengthened by improved histopathology and ultrastructural changes, which specifies the salvage of cardiomyocytes from the deleterious effects of ISO. The present study findings demonstrate that cardamom significantly protects the myocardium and exerts cardioprotective effects by free radical scavenging and antioxidant activities.

Highlights

  • Myocardial infarction (MI) is characterized by an inequity of coronary blood supply and demand, which results in myocardial ischemic injury and damages the cardiomyocytes [1]

  • ISO injections induced a significant decrease in heart rate and systolic arterial pressure (SAP), diastolic arterial pressure (DAP) and mean arterial pressure (MAP) as compared to normal control group (Table 1)

  • Following the administration of ISO, a robust fall in the activities of endogenous antioxidant systems of the heart leads to the gradual loss of pro-oxidant/antioxidant balance that accumulates in cardiomyocytes and manifest as oxidative damage

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Summary

Introduction

Myocardial infarction (MI) is characterized by an inequity of coronary blood supply and demand, which results in myocardial ischemic injury and damages the cardiomyocytes [1]. MI is the most clinically encountered ischemic heart diseases and remains the foremost reason of death and disability worldwide It is manifested by hemodynamic, biochemical and histopathological alternations accompanied with altered arterial pressure indices, heart rate, ventricular impairment, and preload as well as diminished endogenous antioxidants, escape of cardiac injury marker enzymes and lipid peroxidation [3,4]. These changes are consequential to the augmented increase in the ROS such as superoxide anion and hydroxyl radicals in ischemic tissues resulting in oxidative damage to membrane lipids, proteins, carbohydrates and DNA [5]. Numerous synthetic antioxidants have revealed limitations in showing pro-oxidant, toxic and/or mutagenic properties, shifted the attention of researchers towards the naturally derived antioxidants

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