Abstract

The present study was designed to investigate the cardioprotective effects of Malaysian Tualang honey against isoproterenol- (ISO-) induced myocardial infarction (MI) in rats by investigating changes in the levels of cardiac marker enzymes, cardiac troponin I (cTnI), triglycerides (TG), total cholesterol (TC), lipid peroxidation (LPO) products, and antioxidant defense system combined with histopathological examination. Male albino Wistar rats (n = 40) were pretreated orally with Tualang honey (3 g/kg/day) for 45 days. Subcutaneous injection of ISO (85 mg/kg in saline) for two consecutive days caused a significant increase in serum cardiac marker enzymes (creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and aspartate transaminase (AST)), cTnI, serum TC, and TG levels. In addition, ISO-induced myocardial injury was confirmed by a significant increase in heart lipid peroxidation (LPO) products (TBARS) and a significant decrease in antioxidant enzymes (SOD, GPx, GRx, and GST). Pretreatment of ischemic rats with Tualang honey conferred significant protective effects on all of the investigated biochemical parameters. The biochemical findings were further confirmed by histopathological examination in both Tualang-honey-pretreated and ISO-treated hearts. The present study demonstrates that Tualang honey confers cardioprotective effects on ISO-induced oxidative stress by contributing to endogenous antioxidant enzyme activity via inhibition of lipid peroxidation.

Highlights

  • Oxidative stress due to excess production of reactive oxygen species (ROS), along with free radicals, has been implicated in a large number of diseases, including cardiovascular diseases (CVDs), liver diseases, and neurodegenerative diseases including Alzheimer’s and Parkinson’s disease [1, 2]

  • Rats injected with ISO alone showed a marked (p < 0.05) elevation in the serum cardiac troponin I (cTnI) levels when compared to normal controls

  • Oral pretreatment of Tualang honey (TH) to ISOtreated rats for a period of 45 days significantly (p < 0.05) decreased serum cTnI levels when compared with ISO and normal control groups (Figure 1)

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Summary

Introduction

Oxidative stress due to excess production of reactive oxygen species (ROS), along with free radicals, has been implicated in a large number of diseases, including cardiovascular diseases (CVDs), liver diseases, and neurodegenerative diseases including Alzheimer’s and Parkinson’s disease [1, 2]. According to the World Health Organization, MI is the major cause of death in the developed world and a cause of major pathology worldwide. By 2020, MI is predicted to be the major cause of death in the world [6, 7]. Oxidative deterioration of membrane polyunsaturated fatty acids (PUFAs) within the myocardium has been linked to increased levels of lipid peroxides such as thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides (LOOH). These changes occur during the initial stages of MI and increase the tissue’s susceptibility to oxidative damage. This is followed by hyperglycemia, hyperlipidemia, peroxidation of membrane phospholipids, and loss of membrane integrity [4, 8]

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